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JAMA confirms HIV load doesn’t govern CD4 loss


Lynchpin falls out of paradigm

No explanation yet from Dr Fauci, and we think we know why

Interesting JAMA story moving on the UPI ticker just now: HIV measurement is questioned. Seems viral load has little to do with CD4 loss in untreated HIV + patients.

Dr. Benigno Rodríguez of Case Western Reserve University and colleagues conducted a study to estimate the extent to which presenting blood levels of HIV can account for the rate at which CD4 cells are depleted among an untreated HIV-infected population of patients.

The researchers found only a small proportion of the rate at which CD4 cells are lost could be explained by plasma HIV RNA level, suggesting more than 90 percent of the determinants of CD4 cell decline are not reflected in the amount of virus in blood.

So don’t hurry to take HAART just because your HIV count is high. Is that right?

If so, where does that leave the paradigm and Anthony Fauci’s assurance that HIV causes depletion of CD4 cells, directly, indirectly and some other mysterious way as yet undefined but characterised by the paradigm defense team’s head man, Zvi Grossman, as a “conundrum”.

Seems we don’t even have to work out what the conundrum is. HIV doesn’t correlate with CD4 loss, period. Not in untreated patients. Not before HAART messes with your constitution.

Ah well, it’s late, maybe we got it all wrong. But looks to us as if the paradigm is failing on every front. Viral load doesn’t govern CD4 loss. That’s a problem to explain, unless you are a dissenter, ie someone with a few working brain cells left in this field.

Is it time for Gallo et al to pack for Rio? He should buy his ticket, the way things are crumbling.

Still, since Fauci presumably has been forewarned, he probably has an answer for us tomorrow, and Larry will let us know at the Times.

UPDATE: here is an AMA rundown of the paper:

“These findings represent a major departure from the notion that plasma HIV RNA level is a reliable predictor of rate of CD4 cell loss in HIV infection and challenge the concept that the magnitude of viral replication (at least as reflected by plasma levels) is the main determinant of the speed of CD4 cell loss at the individual level. The clinical implications are that in the majority of cases, an individual patient’s plasma HIV RNA level at the time of presentation for clinical care cannot predict, to a significant extent, the rate of CD4 cell decline that he or she will experience over the subsequent years and is therefore of limited clinical value in shaping the decision to initiate antiretroviral therapy,” the researchers write.

(JAMA. 2006;296:1498-1506.)….

“The second and potentially more exciting implication of the findings of Rodriguez et al is that future improvements in the treatment of HIV infection and AIDS may result from improved understanding of the 90 percent of CD4 cell depletion that remains enigmatic,” they write. “A better understanding of the immunologic and genetic factors that drive HIV-associated CD4 cell loss may translate to novel therapeutic approaches that could favorably shift the pathogen-host balance.

So 90 per cent of CD 4 depletion is not driven by HIV? But… but… Dr. Fauci, come to our rescue here. We were under the impression that HIV caused AIDS by depleting CD4 cells. You told the audience that when you appeared in New York with Mathilde Krim and Larry Kramer at the New School to celebrate “AIDS after 25 Years”. Help us here.

Did Dr Fauci censor himself on HIV∫AIDS flaws?

Why was this paper not flagged at NIAID before it could be published? The answer to that question also seems enigmatic. Maybe it was because Dr Fauci thought there might be something in our previous nomination on his behalf for recognition from Stockholm (Dr Fauci finds solution to AIDS – it’s HIV; NAR nominates him for Nobel) on the grounds that he had discovered that HIV actually increased CD4+8 proliferation, and therefore was an antidote to itself.

Readers may note that at the bottom of that post is a Comment by Robert Houston which points out that Dr Fauci himself in a review of HIV∫AIDS quoted from a paper he himself forwarded to the National Academy of Sciences that showed that a huge rise in HIV load of 5,560% resulted in a negligible change in CD4 count of -6%, at the same time as boosting CD8 count 20%.

Is it possible that Dr Fauci is aware of the fact that HIV load has no great influence on CD4 count, and even wrote about it for the information of the medical community, on the basis of a paper he forwarded to the National Academy, and somehow forgot to tell government officials, health workers and the public?

Surely it would be too cynical to imagine that the director of NIAID would censor himself in this way, after censoring the media for twenty two years?

Surely a public servant of the well paid and important kind that Dr Fauci is would never withhold information from members of the public who pay his salary who might then be misled into taking drugs with horrendous side effects for no good reason?

Surely a public servant of the stature of Dr Fauci would not freely acknowledge a flaw in the paradigm which has brought so much funding to his institution among colleagues, and yet somehow neglect to tell the public?

If he did, then it behooves us to wonder just how flawed does Dr Fauci think the HIV∫AIDS paradigm really is. Are there other flaws which he has quietly recognized in chats and talks to his peers in the medical policy fraternity, but has omitted to acknowledge in public?

It already seems clear that his answer to Robert Houston at the “AIDS after 25 Years” panel on how HIV killed CD4 cells was misleading. He repeated the same old claims that there was direct killing and indirect killing which have not only been revealed as specious by mainstream papers which he must have read himself, but he knew himself from his own review and paper that HIV load has very little to do with CD4 count changes.

So today’s revelation in JAMA is nothing new to him, and we don’t really expect him to help us to understand it. Dr Fauci’s policy on informing the public seems to be this: however many reasons there are to doubt that HIV is “the virus that causes AIDS”, it is important not to undermine public confidence by acknowledging them in public.

But it is fine to talk and write about them among colleagues.

We wonder what all the haplessly gullible gays now staggering about with wrecked and ugly bodies, and the ghosts of their dead, will have to say about it when they finally come to their senses?

Maybe they will take up Larry Kramer on his suggestion for a latter day Nuremburg Trial, and put Dr Anthony Fauci in the dock.

AMA rundown:

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Libraries

Medical News

Keywords

HIV, CD4 CELLS, IMMUNE RESPONSE

Contact Information

Available for logged-in reporters only

Description

Preliminary research indicates that the initial HIV RNA level in untreated HIV-infected patients appears to have little value in predicting the rate of CD4 cell count decrease, potentially limiting its clinical value concerning the decision of when to begin antiretroviral therapy for an individual, according to a study in the September 27 issue of JAMA.

Newswise — Preliminary research indicates that the initial HIV RNA level in untreated HIV-infected patients appears to have little value in predicting the rate of CD4 cell count decrease, potentially limiting its clinical value concerning the decision of when to begin antiretroviral therapy for an individual, according to a study in the September 27 issue of JAMA.

Depletion of CD4 cells is a characteristic of progressive human immunodeficiency virus (HIV) disease and a powerful predictor of the short-term risk of progression to AIDS, according to background information in the article. Blood levels of HIV are also thought to predict HIV disease progression risk. In addition to their role as predictors of the clinical outcomes of HIV infection, CD4 cell count and plasma HIV RNA level are commonly used as markers of the success of highly active antiretroviral therapy (HAART). Until this study was completed, however, the degree to which blood levels of HIV could predict the rate of CD4 cell loss in HIV-infected individuals with similar demographic characteristics to those seen in clinical practice was unclear.

To address this question, Benigno Rodríguez, M.D., of Case Western Reserve University, Cleveland, and colleagues conducted a study to estimate the extent to which presenting blood levels of HIV can account for or “explain” the rate at which CD4 cells are depleted among an untreated HIV-infected population of patients including women and ethnic minorities. The study included repeated analyses of 2 multicenter groups, with observations beginning in May 1984 and ending in August 2004. Analyses were conducted between August 2004 and March 2006. The participants included antiretroviral treatment–naïve, chronically HIV-infected persons (n = 1,289 and n = 1,512 for each of the 2 groups) who were untreated during the observation period (6 months or greater) and with at least 1 HIV RNA level and 2 CD4 cell counts available. Approximately 35 percent were nonwhite, and 35 percent had risk factors other than male-to-male sexual contact.

The researchers found that only a small proportion of the rate at which CD4 cells are lost (only 4 percent – 6 percent) in a given individual patient could be explained by presenting plasma HIV RNA level, suggesting that in chronic untreated HIV infection over 90 percent of the determinants of CD4 cell decline are not reflected in the amount of virus in blood at the time of initial medical evaluation.

“Our findings confirm previous observations that the magnitude of HIV viremia [the presence of a virus in the blood stream], as defined by broad categories of presenting HIV RNA level, is associated with the rate of CD4 cell loss and extend this observation to patient populations comprising both men and women. Despite this association, however, only a small proportion of the interindividual variability in the rate of CD4 cell decline can be explained by plasma HIV RNA level, even after accounting for the effect of measurement error,” the authors write.

“These findings represent a major departure from the notion that plasma HIV RNA level is a reliable predictor of rate of CD4 cell loss in HIV infection and challenge the concept that the magnitude of viral replication (at least as reflected by plasma levels) is the main determinant of the speed of CD4 cell loss at the individual level. The clinical implications are that in the majority of cases, an individual patient’s plasma HIV RNA level at the time of presentation for clinical care cannot predict, to a significant extent, the rate of CD4 cell decline that he or she will experience over the subsequent years and is therefore of limited clinical value in shaping the decision to initiate antiretroviral therapy,” the researchers write.

(JAMA. 2006;296:1498-1506. Available pre-embargo to the media at http://www.jamamedia.org.)

“The second and potentially more exciting implication of the findings of Rodriguez et al is that future improvements in the treatment of HIV infection and AIDS may result from improved understanding of the 90 percent of CD4 cell depletion that remains enigmatic,” they write. “A better understanding of the immunologic and genetic factors that drive HIV-associated CD4 cell loss may translate to novel therapeutic approaches that could favorably shift the pathogen-host balance.

Editor’s Note: This work was supported in part by the Case Western Reserve University Center for AIDS Research and NIH grants. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.

Editorial: Explaining, Predicting, and Treating HIV-Associated CD4 Loss – After 25 Years Still a Puzzle

In an accompanying editorial, W. Keith Henry, M.D., of the University of Minnesota, Minneapolis; Pablo Tebas, M.D., of the University of Pennsylvania, Philadelphia; and H. Clifford Lane, M.D., of the National Institute of Allergy and Infectious Diseases, Bethesda, Md., discuss the findings concerning HIV RNA levels and CD4 cell loss.

“The study by Rodriguez et al may have several important clinical implications. The first and more straightforward is that baseline measurements of viral load alone should have less of a role in driving decisions on when to start antiretroviral therapy for an individual patient; these initial viral load levels cannot predict how rapidly the disease will progress. … The seemingly useful practice of combining a CD4 cell count and plasma HIV RNA levels to assess an individual patient’s prognosis for AIDS progression or response to highly active antiretroviral therapy needs reexamination.”

“The second and potentially more exciting implication of the findings of Rodriguez et al is that future improvements in the treatment of HIV infection and AIDS may result from improved understanding of the 90 percent of CD4 cell depletion that remains enigmatic,” they write. “A better understanding of the immunologic and genetic factors that drive HIV-associated CD4 cell loss may translate to novel therapeutic approaches that could favorably shift the pathogen-host balance. … Discovering and developing therapies that target key nonviral factors has the potential over the decades ahead to build on the success of antiretroviral therapy and expand access to sustainable effective therapy.”

(JAMA. 2006;296:1523-1525. Available pre-embargo to the media at http://www.jamamedia.org.)

Editor’s Note: Please see the editorial for financial disclosures, funding and support, etc.

HIV measurement is questioned

(show)

CLEVELAND`, Ohio, Sept. 26 (UPI) — Preliminary U.S. research indicates the HIV RNA level in untreated HIV-infected patients has little value in predicting the rate of CD4 cell count decrease.

Researchers say that potentially limits HIV RNA’s clinical value concerning the decision of when to begin antiretroviral therapy.

Until the new study was completed, the degree to which HIV blood levels could predict the rate of CD4 cell loss was unclear.

To address the question, Dr. Benigno Rodríguez of Case Western Reserve University and colleagues conducted a study to estimate the extent to which presenting blood levels of HIV can account for the rate at which CD4 cells are depleted among an untreated HIV-infected population of patients.

The researchers found only a small proportion of the rate at which CD4 cells are lost could be explained by plasma HIV RNA level, suggesting more than 90 percent of the determinants of CD4 cell decline are not reflected in the amount of virus in blood.

The research appears in the current issue of the Journal of the American Medical Association.

UPDATE: Nick Bennett Replies on his site Viral load paradigm shift? Not really.

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Wednesday, September 27, 2006

Viral load paradigm shift? Not really.

An interesting study came out recently (I managed to get a copy of the article from one of the authors) on the predictive value of viral load. It’s well known (at least among those who bother to read and understand the literature) that those people with higher viral loads tend to progress faster, as was shown by John Mellors back in the mid 1990s using the large Multicenter AIDS cohort study (MACS).

This study took things one step further. They replicated the original findings of Mellors by showing again that viral load roughly predicted how fast AIDS occurred in another large cohort composed of people from 3 seperate study sites. For example, in this new paper people with viral loads less than 500 had an average loss of CD4 cells of 20 per year whereas those with viral loads over 40,000 had an average loss of 78 a year (with a smooth change for values inbetween). Basically this data proved that viral load was a reasonable predictor of rate of progression! They compared this analysis with the original MACS cohort and it looks practically identical!

But then they tried to look at the individual rate of progression of each member of the cohort. Unsurprisingly they found that the rough-and-ready estimates of progression rate within a subgroup varied from one individual to another. When they ran complex statistical analysis on the effects of viral load on THIS data they found that only about 5-6% of the inter-individual variation can be explained by the initial viral load. In another words, while viral load predicts that you WILL lose CD4 count, and you can give an AVERAGE loss of CD4 cells per year based on that count, you can’t say for sure what the ACTUAL loss will be for any one person very accurately.

Well, duh. Nothing amazing there.

Now, what’s sad about this whole thing is that is appears as if the dissident websites have jumped all over the mass-media coverage of this without bothering to read the paper. They are assuming that this somehow negates the usefullness of viral load measurements. Ironically if a paper showing that viral load predicted 100% of the CD4 T cell loss (an impossible thing) relied on complex statistical analysis I’m sure they wouldn’t accept it with anything like the same level of naivity!

This is nothing new – we’ve known for years that various other factors can play into AIDS progression, from nutritional status to immune makeup, depression, and viral genetics. We’ve known for years that overall T cell losses include uninfected as well as infected cells, that immune hyperactivation leads to apoptosis but a lack of renewal – both things that are only indirectly due to HIV infection, but not direct cell killing. What we haven’t done before is put a number on anything – to say roughly HOW much influence these things can have on an individual level.

It should also be noted that this should lay to rest any idea that mainstream science is simply laying back and accepting the current paradigm without question. If that were the case, why was this large, comprehensive, complex study performed? Is it because that when dissidents say that scientists ARE sitting back on the current paradigm they are…*gasp*…lying??! And, SHOCK HORROR, this was supported by an NIH grant, the very same NIH that the dissidents are trying to claim is horribly corrupt and under the thumb of pharmaceutical sponsors!

Ahh, is that the sound of cherries being picked?

Anyhow, I will quote from the paper:

“Our findings confirm previous observations that the magnitude of HIV viremia, as defined by broad categories of presenting HIV RNA level, is associated with the rate of CD4 cell loss and

extend this observation to patient populations comprising both men and women.”

In other words, viral load predicts rate of progression to AIDS.

If the dissidents are trying to twist this paper to say anything else, they are managing a feat of astonishing deception. Is there more to the story? Of course! No-one, except the dissidents, is saying anything else. They also state that “In humans, the predictive value of immune activation level on HIV disease course, independent of plasma HIV RNA levels, can be demonstrated even when measured during early infection”, which goes back to what I said above.

And I refer the reader to my older post on HIV pathogenesis.

It should also be mentioned that viral load isn’t used as a clinical criteria for starting treatment unless the load is very high and the CD4 counts are equivocal. Viral load is almost exclusively used for monitoring response to therapy on the individual level, so inter-individual variability isn’t an issue anyway.

This result is very important in that it highlights the need to investigate other factors important in triggering or controlling rate of progression to AIDS, but it won’t really change the current paradigm in terms of understanding AIDS pathogenesis, nor will it change current treatment guidelines, because neither depends on the idea that HIV viral load is the be-all and end-all of AIDS.

Except of course, that it is in the minds of the dissidents.

Which is (one reason) why they’re wrong.

posted by Bennett at 11:18 PM

0 Comments:

Comment: Bravo, Bennett, for defending the paradigm against what looked like a nasty finding judging from the first reports. Now we too have the actual paper in hand, we can see that the point Dr Bennett makes is perfectly correct, this was a paper dealing with variations between individual experiences, not with the overall correlation between the two measures of HIV and CD4 for all the patients in the study. Naturally there can be many other factors accounting for variations in individual experience, as there are many reasons for contracting AIDS symptoms, and reasons for vulnerability.

But he entirely overlooks the thrust of the paper, which demonstrates that the authors are unable to discern what those causes of variation might be. They explored the possibilities that sex, risk factor and/or presenting HIV RNA stratum might be the answer and found nothing that could predict the rate of CD4 loss. In fact, Bennett’s reassurance that everything is fine in HIV∫AIDS la la land is merely the same old reflex denial of the big black headline over the AMA comment by W. Keith Henry, which is that “Explaining, Predicting and Treating HIV-Associated CD4 Cell Loss (is) After 25 Years Still a Puzzle.

Henry et al note that the report “challenges the notion that, at the individual level, a limited number of HIV measurements over a short period of time provide meaningful prognostic information regarding the rate of CD4 cell decline and by extension the risk of opportunistic infections.” Of course, if the medical fraternity would take off their NIAID provided glasses with “HIV is behind everything” etched onto them they would have known this in the first place. If they bothered to read their own literature (or this blog) or even think clearly they would know that it is just as likely that CD4 counts are lower at rest and higher when activated, than vice versa, as Dr Fauci has recently touched on in his extensive review. Moreover, the level of active virus in the blood of patients without AIDS symptoms in the long “latent period” is utterly negligible. It is hard to conceive it has anything at all to do with changes in CD4 count, compared with myriad other influences on the immune system.

The result of the study is in fact utterly predictable, and the only surprise it holds is for those who imagine that the simple minded mechanism of HIV causing AIDS imagined in the first place over two decades ago – HIV killing CD4 cells dirctly – is still part of the paradigm. This includes Dr Fauci, it appears, who doesn’t read his own medical literature according to his public statement at the New School on the ways HIV kills CD4 cells, which repeated this now outmoded idea, as well as the cell suicide theory of “indirect killing”, when both are rejected by his top theoretical thinker Zvi Grossman, who has retreated to the conclusion that how it all happens is a “conundrum”.

What is really the study’s only novel usefulness is its demonstration yet again that no one has any idea how HIV can possibly govern the loss of CD4 cells that is held to be cause of AIDS, and that the obvious alternative – that HIV is merely an opportunistic infection, and rather than governing CD4 count, it is CD4 count that governs the rise and fall of HIV viral load, as CD4 numbers are affected by other factors – the poisons and other assaults that may bring on AIDS symptoms.

It puts yet another nail in the coffin of a paradigm that has never been able to demonstrate its central premise.

184 Responses to “JAMA confirms HIV load doesn’t govern CD4 loss”

  1. German Guest Says:

    No, no, they must be completely 100 % wrong. CD4 cells are destroyed by HIV, the virus that causes AIDS. I chose to believe because the scientific evidence is absolutely overwhelming!

    Charles Farthing, MD – Medical Director of the AIDS Healthcare Foundation (2005 HIV Leadership Award winner):

    “The people who say that HIV is not the cause of AIDS are practicing supreme denial. It is amazing how human beings can look at black and call it white or look at white and call it black. They can look at all the symptoms but if they don’t chose to believe it – they don’t chose to believe it.
    Many human beings are not rational, they don’t operate on logic – they operate on emotions. And that’s exactly what those people are doing. They don’t want to believe it, so it’s not the case. But unfortunately, they’re completely 100 % wrong. There is no doubt that HIV causes AIDS. The scientific evidence is absolutely overwhelming. But if you chose to ignore it, of course, you can ignore it.”

    (2004, http://www.theothersideofaids.com, google video)

  2. try_harder Says:

    I was trying to locate this article but had no luck. Have you managed to get hold of it?

  3. try_harder Says:

    Sorry I did find a summary here:

    http://jama.ama-assn.org/cgi/content/abstract/296/12/1498

  4. noreen martin Says:

    We operate in denial and don’t choose to believe it.

    We don’t choose to believe it when our blood and liver enzymes are normal for a change, when we can go to the bathroom like a normal person and when we have no symptoms whatsoever. Now, you tell me who is in some sort of denial here.

    I guess that it would be hard for these people to admit to a mistake, especially since being highly educated, they have believed it and prescribed toxic medicines for the most part,needlessly for over twenty some years.

    This fortress or Aids Wall is crumbling all around em; they need to regroup and maybe change their position in life.

  5. reniori Says:

    TS wrote:

    “HIV doesn’t correlate with CD4 loss, period”

    Wrong, TS. It does indeed correlate with CD4 loss. The article you are referring to does not question that correlation — that’s just the math of it — it suggests that the correlation is SPURIOUS. There is a difference between a zero-order correlation (no relationship) and a spurious one (where correlation is an artifact of some other variable.

  6. Dan Says:

    As much as this rightfully sounds like yet another nail in the coffin of the paradigm, we should know by our past experience that this will have little or no effect on the great minds that work tirelessly on trying to solve the “AIDS crisis”. As long as they maintain that “HIV causes AIDS”, contradictions, paradoxes, and illogic make happy company.

  7. German Guest Says:

    look here for more detailed information about the paper!

    An accompanying editorial in the same issue of JAMA by Dr Keith Henry from the University of Minnesota and colleagues from the University of Pennsylvania and the National Institute of Allergy and Infectious Diseases, calls the study’s findings “provocative” and notes that “25 years into the HIV epidemic, a complete understanding of what drives the decay of CD4 cells – the essential event of HIV disease – is still lacking.”

  8. pat Says:

    “Wrong, TS. It does indeed correlate with CD4 loss. The article you are referring to does not question that correlation — that’s just the math of it — it suggests that the correlation is SPURIOUS.”

    Is this the momentum of denialism on display?

  9. Dan Says:

    “The second and potentially more exciting implication of the findings of Rodriguez et al is that future improvements in the treatment of HIV infection and AIDS may result from improved understanding of the 90 percent of CD4 cell depletion that remains enigmatic,” they write. “A better understanding of the immunologic and genetic factors that drive HIV-associated CD4 cell loss may translate to novel therapeutic approaches that could favorably shift the pathogen-host balance.

    Leave it to the researchers to completely avoid the obvious. Got to love that word, “enigmatic”. It’s right up there with cunning, wily, elusive, mysterious, and all other such words that get used, instead of questioning the most basic (fatally-flawed) premise – HIV causes AIDS.

    So, quick to turn lemons into lemonade, they find ways to make money from their stupidity (quotes in bold) and the pharmaceutical companies happy.

  10. Chris Scheuermann Says:

    SPURIOUS DEFINITION: 1) Lacking authenticity in essence or origin; not genuine; false. 2) Counterfeit or phony.

    I could go on but everyone can look it up for themselves if they would like to. I was just trying to understand Pat’s post. If he/she were being sarcastic, then you can disregard this post. However, it does not seem that way to me given the last line of the post. So, that being said Pat is arguing that there is indeed a correlation but that it is spurious. So, that is a FALSE correlation. I don’t exactly know how strong an arguement that is. To my way of thinking, not very. And my second point Pat…THE MATH IS EVERYTHING!!

  11. German Guest Says:

    “In a related JAMA editorial, physician W. Keith Henry and colleagues write that the study results are stimulating and suggest that researchers should seek to identify nonviral factors that might trigger the decline of CD4+ T cells (Reuters, 9/27).”

    The Body – HIV Viral Load Is Not Reliable Indicator for CD4+ T Cell Counts

    “nonviral factors” – Well, this a remarkable statement and a real breakthrough in orthodox HIV/AIDS research. Unfortunately, it’s much too late for those who died of AIDS during the past 25 years.

  12. Dan Says:

    German Guest,

    I’d like to think that this was an admission that they’ve been barking up the wrong tree. But “AIDS” is a bizarro world, where down is up, and white is black.

    Even if we go along with this admission that “non-viral factors” may account for the 90% CD4 cell loss that remains “enigmatic”, we’re still unfortunately stuck inside the looking glass of the paradigm. It’s just incredibly strained at this point, though.

    HIV is still part of the equation, and CD4 cell depletion still equals “AIDS”. The only thing that’s changed is that they’ve added the word “enigmatic”. It’s almost humorous (if it weren’t so grim) how far they’ll stretch to keep “HIV” and “AIDS” together.

    All in all, I believe this will turn out to be another of the many dead ends in “AIDS” research (as it comes much to close to toppling their house of cards). Whatever became of the information from that study from UC Davis where the researchers found that HAART is hugely ineffective as “HIV hides in the gut”? Whoops, lost down the “AIDS” memory hole.

  13. Dan Says:

    Somebody should pay me the big bucks!

    I just figured out the explanation for that “enigmatic” loss of CD4 cells. They haven’t taken into account all of that HIV that hides in the gut!! It’s hiding there, munching on T cells, or convincing them to commit suicide, or whatever it does to lessen their numbers. Where’s my check?

  14. kevin Says:

    This a very important finding; everybody reads JAMA. To see such a headline in mainstream press is encouraging. Here’s another link:

    http://news.bbc.co.uk/2/hi/health/5380646.stm

    Looks like they are finally admitting that “viral load” is a meaningless measurement for predicting the health of HIV+ people. Will they ever admit the harm caused to those who started anti-viral treatment early; those without symptoms– many who just wanted to say that they have an “undetectable” level of viral load in the copy of their personals ad, even though they look half-dead from the toxic treatment in the accompanying photos. What about that tragedy. So many tragedies…

    So if viral load is not a good predictor of CD4 loss, which is the crux of their immune suppression theories (all of them), does that mean that HIV loses some credibility as the offending agent? Well, it should for anyone with half a brain. My favorite quote, along those lines:

    “Instead, the findings suggest the factors governing disease progression are rather more complex, and may include damage that HIV is able to inflict on the immune system in an indirect way.”

    Convoluted bullshit-per usual i.e. “May include”, that’s nice…HIV “may” be responsible…OK, as long as your sure. Oh and “indirectly”–do you mean indirectly as in a divine mystery or as in beyond discovery even after 25 years and billions of dollars wasted?

    Kevin

  15. Dan Says:

    From German Guest’s body.com link…

    The study also suggests that predicting disease progression — which is “crucial” in deciding when to start highly active antiretroviral therapy — might be “more complex” and could include indirect ways HIV can harm the immune system, according to BBC News.

    Indirect ways HIV can harm the immune system?

    It looks like they really are getting desperate!!

    So, 22+ years of HIV/AIDS and NOW they’re trying to find “other ways” HIV can harm the immune system? Is this the greatest tragedy/comedy medicine has ever known? This just simply reeks of desperation.

  16. kevin Says:

    Exactly, Dan. Looks like we were on the same page at the same time, literally 😉 It is a true Tragi-comedy, which I’ve always held in less esteem than a good Drama. After all, the true tragedies of life- those beyond our control- are rough enough without creating pain and suffering, en masse. What a dysfunctional society we have become…

  17. Chris Noble Says:

    Have any of you actually read the JAMA paper?

    Look at figure 1.

    Can any of you explain it?

    “Our findings confirm previous observations5 that the magnitude of HIV viremia, as defined by broad categories of presenting HIV RNA level, is associated with the rate of CD4 cell loss and extend this observation to patient populations comprising both men and women.”

    Chris Noble

  18. kevin Says:

    One more thing…I love the graphic with the BBC article…the one declaritively subtitled “HIV attacks immune cells”. How can you have a graphic illustrating that “attack” when the supporting article suggests that attack is indirect. I guess an “indirect” graphic might be misleading and cause misunderstanding, lol.

  19. kevin Says:

    Have any of you actually read the JAMA paper?

    Look at figure 1.

    Can any of you explain it?

    I’m not a paying member of JAMA; therefore, I have only read excerpts and the abstract. I’d love to see the entire article if you have access to it.

    Kevin

  20. Dan Says:

    Our findings confirm previous observations5 that the magnitude of HIV viremia, as defined by broad categories of presenting HIV RNA level, is associated with the rate of CD4 cell loss and extend this observation to patient populations comprising both men and women.

    It’s beginning to smell a lot like Padian…

    These findings represent a major departure from the notion that plasma HIV RNA level is a reliable predictor of rate of CD4 cell loss in HIV infection and challenge the concept that the magnitude of viral replication (at least as reflected by plasma levels) is the main determinant of the speed of CD4 cell loss at the individual level. The clinical implications are that in the majority of cases, an individual patient’s plasma HIV RNA level at the time of presentation for clinical care cannot predict, to a significant extent, the rate of CD4 cell decline that he or she will experience over the subsequent years and is therefore of limited clinical value in shaping the decision to initiate antiretroviral therapy,” the researchers write.

    Like Padian, the first paragraph assures us that they have no intention of rocking the boat. Oddly enough, their findings (second paragraph) do just that. Just a little bit of schizophrenia from our friendly “AIDS” researchers, it seems.

  21. Chris Noble Says:

    It’s beginning to smell a lot like Padian…

    If by this you mean that “rethinkers” deliberately misrepresent these findings then you are 100% correct.

    Figure 1 from the paper shows clearly that if you take a large number of HIV infected people and divide them into groups according to their HIV RNA levels you find that on average people with lower than 500 HIV RNA copies /ml had small decreases in CD4+ counts per year and on average people with viral load above 40000 had much larger decreases in CD4+ cells per year. There is a simple relationship on average between viral load and rate of CD4+ cell depletion.

    What the paper does say is that for one particular individual viral load measurements are not a good predictor of the rate of CD4+ cell depletion.

    It is pure “rethinker” spin to imply that this paper demonstrates that there is no relationship between viral load and CD4+ cell depletion.

  22. Dan Says:

    It is pure “rethinker” spin to imply that this paper demonstrates that there is no relationship between viral load and CD4+ cell depletion.

    Oh, Chris,

    this one’s going to just suck for you.

    All I did was point out some schizophrenia. The first paragraph toes the party line. The second one, well, looks a bit damning for the party line. Folks can decide for themselves.

    P.S., yes, it really looks like bad news for the relationship between viral load and CD4+ cell depletion.

  23. Chris Noble Says:

    P.S., yes, it really looks like bad news for the relationship between viral load and CD4+ cell depletion.

    Have you looked at Figure 1 yet?

    Can you explain it?

  24. German Guest Says:

    @ Chris Noble:

    “The researchers found that “the viral load for the individual has very little predictive value in terms of how rapidly a person is going to progress to AIDS,” said Rodriguez.

    In fact, he added, “In our study, we had about 10 percent of patients with low viral loads that had extra rapid disease progression, so people should know that having a low load doesn’t mean you’re OK.”

    Link: medicinenet

    CAN YOU EXPLAIN IT???

  25. Chris Noble Says:

    Read the paper!

    On average people with low viral load have slow progression and people high high viral load have fast progression.

    One of the authors of the study has made this comment.

    “The idea that our findings published today in JAMA can be taken to support the concept that HIV is not the cause of AIDS is ludicrous. The role of HIV as the cause of AIDS has been proven over and over again. Clearly the people who are misrepresenting our work are not only incapable of clear thinking, they are also apparently unable to read.”
    Michael M. Lederman MD

    Although on average people with low viral load have a smaller yearly decrease in CD4+ cells and on average people with high viral load show faster progression this paper demonstrates that there are other important factors that independently determine CD4+ cell depletion rates.

    In humans, the predictive value of immune activation level on HIV disease course, independent of plasma HIV RNA levels, can be demonstrated even when measured during early infection47 or before actual seroconversion. 48 Thus, immune activation may be a major determinant of T-cell turnover and CD4 cell depletion in chronic HIV infection49 both in human and animal hosts.

    Still as yet none of the “rethinkers” has yet made a comment about figure 1 in the JAMA paper and the implication it has for the claim that HIV has nothing to do with the progressive loss of CD4+ cells.

    Look at the figure! Viral load is directly correlated with the rate of CD4+ cell depletion! It is right there staring at you.

  26. German Guest Says:

    @ Chris Noble:

    One of the authors of the study has made this comment.

    “The idea that our findings published today in JAMA can be taken to support the concept that HIV is not the cause of AIDS is ludicrous. The role of HIV as the cause of AIDS has been proven over and over again. Clearly the people who are misrepresenting our work are not only incapable of clear thinking, they are also apparently unable to read.”
    Michael M. Lederman MD

    I can’t find this statement. Any references would be appreciated.

  27. Chris Noble Says:

    The comment was given to Nick Bennett in a personal communication.

    http://tinyurl.com/nxxow

    If “rethinkers” really believe that the article should be interpretted in the manner that they think then they could at least contact the authors of the article.

    It is ludicrous to imagine that people with no relevant scientific experience can interpret the data better than the authors themselves.

    But really, to anyone that claims that this paper is evidence that HIV does not cause AIDS please explain figure 1 that clearly shows a correlation between viral load and CD4+ cell depletion. Complete coincidence?

  28. MacDonald Says:

    There’s a clear correlation between smoking and higher rates of HIV infection. Complete coincidence?

    Or does smoking cause HIV?

  29. German Guest Says:

    @Chris Noble:

    The comment was given to Nick Bennett in a personal communication. http://tinyurl.com/nxxow:

    “I have permission to quote from the paper’s author, when he found out that the AIDS dissidents were hijacking his work.”

    I understand. That’s what you call scientific evidence??? *Laughing out loud!* This is ridiculous.

  30. Dan Says:

    Chris,
    let’s put this in perspective…

    This is just one study. Like Padian’s (for those of us whose minds haven’t been rotted into a convoluted belief system, and are able to think critically and rationally), it makes a thinking person go “hmmmm”.

    Don’t worry too much, Chris. Your beloved paradigm is still standing (for the moment). As long as researchers can publicly engage in cognitive dissonance and it goes unquestioned (except by rethinkers), you can rest easy.

  31. Lise Says:

    Mr. Noble, allow me to rephrase Mr. MacDonald:

    There’s a clear correlation between yellow fingers and high reates of HIV infection. Complete coincidence?

    Or do yellow fingers cause HIV infection?

  32. Martel Says:

    Chris is right. Take a look at figure 1.
    All the authors are saying is that the correlation–while obviously there–isn’t strong enough to merit making clinical decisions based SOLELY upon viremia.
    As for “indirect effects” reflecting desperation after decades of research, scientists have been studying these indirect effects for many years. Look up cytokines and inflammation on Wikipedia or somewhere if you want more info.
    This paper sheds some light on the fallacy of using viral load as a be-all-end-all indicator. No more and no less.

  33. noreen martin Says:

    Maybe I am a little old-fashioned, but why can’t they just go by the patient’s symptoms and forget CD4’s and viral loads. I guess if they were to do that, they would put themselves out of the Aids business. I would personally stack my CBC count up against any one who is on the HAART.

    I am revamping my website and in the future will be posting my bio, lab reports, photos, etc. to show how well one can do without the HAART.

  34. Lise Says:

    ‘No more and no less’. How could it be ‘more’?

    This ‘fallacy’ has governed clinical decisoins and justified general policy for years.

  35. Dan Says:

    Maybe I am a little old-fashioned, but why can’t they just go by the patient’s symptoms and forget CD4’s and viral loads. I guess if they were to do that, they would put themselves out of the Aids business.

    You did a good job of answering your own question, Noreen.

    If we actually went by the patient’s symptoms, that would basically put us in the pre-’93 definition of “AIDS”. It would drastically cut the number of “AIDS” cases here in the U.S. As you might already know, when the definition of “AIDS” changed in ’93, the number of “AIDS” cases doubled.

  36. Truthseeker Says:

    Note: Nick Bennett’s apologia for this paper is now appended at the end of the post with a Comment rejecting it.

  37. German Guest Says:

    As Chris Noble feels authorized to quote from thirdparty “personal communication with the paper’s author” I feel indeed entitled to quote Dr. Pablo Tebas, an associate professor of medicine at the University of Pennsylvania, who with two other AIDS doctors wrote an accompanying editorial in JAMA:

    “Over time, we have realized that viral load doesn’t tell the whole story. It gives us a different perspective and shows us how much we don’t know about how this disease progresses. This study suggests that we need strategies based on the immune system and the person, not just the virus.”

    HIV test in doubt

    How long will it take, until they “discover” that AIDS-patients need a change in lifestyle, rebalanced immune systems and individual conventional treatment for each opportunistic disease?

  38. noreen martin Says:

    How long will it take before they “discover that Aids patients need a change in lifestyle”, rebalanced immune systems and individual conventional treatments for each opportunistic disease?

    It probably will be a very cold day in hell when they revert back and do this as they will have to admit that they were wrong and patients were needlessly killed.

    The above was well stated, the cure for Aids is so simple that it is overlooked or not even acknowledged as the cure. I am always amazed that my infectious disease doctors don’t even ask me “how” I am doing so well. I wonder what is going on in their brains to see a non-drugged person alive and well. Anyway, the ball is in my court now.

  39. Bialyzebub Says:

    Let it never be said of me that I am nothing if not an equal opportunity spitball and heater down the middle pitcher.

    These sentences of the sometimes errant, but also sometime right on, TS are in the latter categories and I commend them, with no tongues in any cheeks, to all and sundry, in particular to the die hardest defenders of their church. In fact they should convert it into a special chorus to their favorite hymn that they sing often enough but never seem to understand — correlation is not causation.

    “What is really the study’s only novel usefulness is its demonstration yet again that no one has any idea how HIV can possibly govern the loss of CD4 cells that is held to be cause of AIDS, and that the obvious alternative – that HIV is merely an opportunistic infection, and rather than governing CD4 count, it is CD4 count that governs the rise and fall of HIV viral load, as CD4 numbers are affected by other factors – the poisons and other assaults that may bring on AIDS symptoms.”

  40. Chris Noble Says:

    In fact they should convert it into a special chorus to their favorite hymn that they sing often enough but never seem to understand — correlation is not causation.

    What Bialy really means is that correlation is not causation except when I say it is.

    When Bialy claims that AZT increases the risk of AIDS by a factor of 4.5 he is saying that correlation is causation.

    Bialy should follow his own advice.

    In this recent paper in JAMA they found a clear and consistent relationship between viral load and the rate of CD4+ cell depletion. Look at figure 1.

    Anybody that ignores this is being dishonest.

  41. Robert Houston Says:

    Perhaps Mr. Noble should endeavor to display more of the honesty that he nobly recommends by confronting the main finding of the new JAMA study by Rodriguez et al. This was the miniscule amount of CD4 variability that can be accounted for by the HIV values. Figure 1, which he keeps pointing to, depicts an association of HIV ranges with CD4 declines. It does not tell us the amount of association when all the cases in the group are considered. As the authors state in their abstract:

    “Despite this trend across broad categories of HIV RNA levels, only a small proportion of CD4 cell loss variability (4%-6%) could be explained by presenting plasma HIV RNA level.”

    Figures 2 and 3 show that there is considerable dispersion around the values shown in figure 1. As the JAMA editorial notes, “In many cases it is difficult to elucidate what is cause and what is effect in these observations.” They also point out that, “The findings by Rodriguez et al provide support to those who favor nonvirological mechanisms as the predominant cause of CD4 cell loss.”

  42. Chris Noble Says:

    Figures 2 and 3 show that there is considerable dispersion around the values shown in figure 1.

    I never claimed there wasn’t. Obviously factors other than serum viral load by itself are important in determining the rate of CD4+ cell depletion. HIV viral load by itself is not a good predictor of progression. Nonvirological factors such as the level of immune activation are suggested as probable determining factors.

    As direct killing has not been thought to be the dominant mechanism in which HIV causes CD4+ cell depletion for over a decade this is hardly a problem.

    The results that on average show a clear and reproducible relationship between HIV viral load and CD4+ cell depletion rate do, however, present a huge problem for people that claim that HIV has nothing whatsoever to do with CD4+ cell depletion.

    Why should there be any relationship whatsoever between the amount of HIV and the observed rate of CD4+ cell loss in untreated people? Any theories? Or will you simply choose to ignore this inconvenient observation?

  43. Truthseeker Says:

    Perhaps Mr. Noble should endeavor to display more of the honesty that he nobly recommends

    Distinguished posters here should remember that accusations of dishonesty are inappropriate on NAR, since the only possible reason that Commenters do not follow the lucid explanations of the posts is that (as in this case, it is clear) they have not read or understood them, or that they are not intelligent enough to understand a point (which good manners should prevent anyone here from mentioning), and NOT that anyone is being dishonest, or poorly motivated.

    Since there are clearly varying levels of intelligence and expertise at work here, with some distinguished posters clearly more attentive and able to grasp matters more readily than others, it is only fair to be kind in one’s manner to all who may overlook some point which one oneself think is blindingly obvious, but which they fail to recognize even after repetition.

    This particularly applies to those who may not understand the literature correctly when it is published, since after all it is often written in a fashion designed to prevent the prying eyes of paradigm critics or any other nosy outsiders from appreciating that the results of the work bring the paradigm into serious or fatal question.

    Why should there be any relationship whatsoever between the amount of HIV and the observed rate of CD4+ cell loss in untreated people? Any theories? Or will you simply choose to ignore this inconvenient observation?

    Chris, what is it about the conclusion of the post – or Dr Beeb’s unusually appreciative comment for that matter – that you do not understand?

  44. Lise Says:

    In this recent paper in JAMA they found a clear and consistent relationship between viral load and the rate of CD4+ cell depletion

    Mr. Noble,

    A clear, consistent, reproducible relationship between yellow fingers and rate of HIV infection has been found in a recent paper (see the post immediately following this one). I think it is very dishonest of you to ignore this much more important finding.

  45. Truthseeker Says:

    The results that on average show a clear and reproducible relationship between HIV viral load and CD4+ cell depletion rate do, however, present a huge problem for people that claim that HIV has nothing whatsoever to do with CD4+ cell depletion

    The problem is non existent, according to the paper itself. The point being made here, Chris, in this thread and post, courtesy of your reasonable enquiry, is that the clear negative overall HIV-CD4 correlation apparently visible to the naked eye in the two slopes of Fig 1 of the paper, ie the more HIV, fewer CD4 cells, and vice versa, less HIV, more CD4 cells, is less than meets the eye, a broad correlation involving a barely significant change in CD4 count (60 cells higher annual loss if HIV level is 80 times higher), where it is entirely unknown if there is any meaningful causation involved, or any indication which direction that causation if any might take. This is why the key observations and conclusions in the paper express a seemingly entirely contradictory finding of virtually negligible correlation and necessary causation and no guidance at all as to direction.

    As we have stated that you have to read the paper and see that the estimates of Figure 1 are overall trends involving so many factors that the correlation is not necessarily linked by any causation at all. In fact as the paper states after careful analysis there emerges that there is on an individual basis only the very tiniest association between the two – some 4-6% (9% see fig 3d emerges after only after massaging which the authors thmselves admit is unrealistic in practice, since it is after the fact).

    As we are all aware a lot of HIV∫AIDS facts and especially those which which are problematic for the paradigm are discreetly curtained off behind statistical adjustments which enhance accuracy and reduce public curiosity and media understanding. Luckily the independent analysts on the staff of NAR are fully versed in the basic methodological and statistical manipulations in the skill set of writers of top level scientific papers, which so conveniently screen their content from independent examination by members of the general public whose welfare is often at stake

    In this case for example we have looked carefully at Figure 2 and can report after massive methodological and factual analysis and reinterpretation using our two supercomputers at full tilt here for several hours (in order to substract -37 from -52) that the correlative analysis of the point at issue boils down to this central fact revealed in Figure 2:

    There is “extensive overlap” in the CD4 outcomes at different HIV levels and that the change is “slight”, as the authors say. In fact it is negligible. A 1000 fold increase in the HIV level is associated with a decrease in the median CD4 count of only 15 cells per year – a change of only 3% of the average CD4 count of 525.

    “Minimal” indeed A dose of corticosteroids as Robert Houston referenced earlier in Comments to the NAR nominates Dr Anthony Fauci for Nobel – he has found the solution to AIDS post where he mentioned the signal review by Al-Bayati, results in a drop in CD4 cell count from 900 to 300 in a matter of ten days. THAT is what we call a significant indication of cause.

    As the JAMA editorial notes the direction of cause and effect is not discernible and the lesson for any sensible person not infected by the AIDS meme is that we have to look for non virological causes as the factors behind CD4 loss.

    What this means in plain English Chris is the flashing sign EXIT PARADIGM.

    Chris, you are the last guy to get the news it seems, but what we are constantly trying to tell you is that you are in effect now riding in an ancient prop driven Stealth Paradigm built in 1984 out of scrap metal and loose wiring flying on instruments through a lightning storm at 40,000 feet which is still has plenty of fuel but in the last few years has had its tail fins and most of its wings shot off, and is piloted by a pilot who is blind in one eye and cannot read the instruments that tell him he is in a steep dive.

    Time to put on the parachute, Chris. The sign is flashing.

  46. Chris Noble Says:

    A clear, consistent, reproducible relationship between yellow fingers and rate of HIV infection has been found in a recent paper (see the post immediately following this one). I think it is very dishonest of you to ignore this much more important finding.

    Who’s ignoring it?

    The author’s of the study in STI also provide plausible explanations for the apparent relationship between smoking and HIV infection risk. They aren’t trying to pretend that the relationship isn’t there.

    On the other hand “HIV rethinkers” are desperately scrambling to deny the implications of the results of this paper in JAMA.

    Studies from two different cohorts show a reproducible relationship between HIV viral load in sub groups and the rate of CD4+ cell depletion.

    You can argue that the relationship is not causal but it is dishonest to claim that the relationship does not exist at all. The data is there and you were all initially happy to trumpet the study before you knew the details. It is dishonest to pull one finding out of the study and then to ignore the data from which it is based.

    Again you can argue that the relationship is not causal but you should at leats attempt to provide an explanation that accounts for the correlation. After all a theory is supposed to account for all the available data and not just bits here and there cherrypicked form different papers while ignoring the vast majority of data.

    So one more can anyone provide a possible explanation of the relationship between HIV viral load and CD4+ cell depletion. Please don’t simply deny the data.

    Chris Noble

  47. Chris Noble Says:

    The problem is non existent, according to the paper itself.

    No.

    Take the relationship between the height of people and their gender.

    Can you measure the height of a person and predict their gender? No. Well at least not reliably. Other factors like ethnic origin are likely to be more important factors in determining height.

    Does this mean that gender has nothing to do with height? No.

    Clearly if you take a random group of women and a random group of men and calculate an average height you will see a significant difference. On average men are taller than women even though there are some women that are taller than the majority of men and there are some men that are shorter than the majority of women.

    Likewise there is a clear and consistent relationship between HIV viral load and CD4+ cell depletion rate. On average people with low viral load show much slower progression than people with high viral load. The error bars in figure 1 in the JAMA paper show that this difference is significant and not due to chance.

    As far as I can tell the theory put forward by Duesberg would predict no relationship whatsoever between HIV viral load and CD4+ cell depletion.

    If his theory or any other “rethinker” theory does predict these observations then please explain how.

    Chris Noble

  48. noreen martin Says:

    Chris, you are assuming that viral loads mean something to begin with. Most “rethinkers” do not believe that they do. However, I will play the devil’s advocate and concede that the HAART will bring the viral load down or to non-detectable and when this happens, yes the CD4’s generally will rise. But having said that, many other things have to come into play here beside these 2 tests. What other levels are being affected by these drugs and what is the quality of life for the patients?

    I have been on all sides of this issue and can state from experience that even being off the meds, having viral loads go up and CD4’s go down, my health is excellent. I believe that these 2 tests are not very good indicators of one health. The symptoms or OI are the thing to worry about. Aids patients have died with high CD4’s and with low CD4’s, so they are not the key ingredients. If we treat problems (as was always done prior to Aids) when they arise, Aids patients would fare that much better and have a chance to rebuild their immune systems which is what has gotten them in this mess to start with in life.

  49. Lise Says:

    As far as I can tell the theory put forward by Duesberg would predict no relationship whatsoever between HIV viral load and CD4+ cell depletion.

    If his theory or any other “rethinker” theory does predict these observations then please explain how.

    Chris Noble

    Dearest me Dr. Noble,

    I didn’t believe in you when my husband first told me. But I see now that for once he wasn’t exaggerating.

    Allow me to paraphrase Mr. Truthseeker this time: what part of the apparently gp120 challenged info-carrier word SURROGATE MARKER is it that reaches your AIDS meme cells in knobless condition so it cannot hook on and penetrate?

    But really you should be more confident in yourself and your analytical abilities. Your own answer was just as good: complete coincidence

  50. Truthseeker Says:

    So once more can anyone provide a possible explanation of the relationship between HIV viral load and CD4+ cell depletion. Please don’t simply deny the data. ….

    As far as I can tell the theory put forward by Duesberg would predict no relationship whatsoever between HIV viral load and CD4+ cell depletion.

    Chris, for the benefit of onlookers one can only repeat that you are contradicting the study authors, who are explicitly perplexed by the little association they found between CD4 cell count and HIV viral load. There is no causal meaning in the broad Figure 1 correlation, even if the numbers are statistically significant; it cannot say anything about causation or the direction of causation because there are too many possible influences on CD4 level operating, and there is no reason not to follow the conventional interpretation that CD4 loss permits HIV load escalation, just like any opportunistic infection.

    We have to accept the work done by the authors that they say shows that HIV can only account for 4% (in their cohort, 6% in the previous cohort they analyzed) of the decline in the CD4 cells. Up to 96% cannot be accounted for by the rise in HIV burden.

    You know perfectly well what the “theory” of Duesberg would be, the alternative hypothesis of a scientist who originally merely pointed out the impossibility of the HIV∫AIDS paradigm, but was forced, without being provided one cent in funding to carry out new research, to provide a corrected version of what was happening in GRID or AIDS, and did so, and no one has yet been able to show any inconsistency in his interpretation. It would be that HIV would behave like any other not very virile opportunistic infection and flourish briefly in any normal immune system according to the vigor of the immune response, which in a normal state of health would generate the extra cells necessary to defeat the invasion in a short time, and would behave less effectively when impacted by any other assaults. He never denied CD4 count went down in patients, but ascribed it to drugs, etc, not HIV, which he denied was a sine qua non of AIDS immune decline. Now this study says he was and is right. It is hardly involved or not involved at all.

    To repeat, the apparently matching slopes of Figure 1 are not valid as a basis for discussion of causation because matching trends can be produced by all kinds of factors, without any causality. When the proper calculation is made, the authors tell us that only 4-6% of the later CD 4 loss is explained by the level of presented virus. As the summary states that’s 4-6% of CD4 loss variability from “HIV RNA levels of 500 or less, 501 to 2000, 2001 to 10,000, 10,001 to 40,000, and more than 40,000 copies per ml” which yield CD 4 losses per year of 20, 39, 48, 56 and 78 cells per ml respectively. 1-3 cells a year! Is that the basis of a global pandemic? On the contrary, it suggests that CD4 cells are immune to the influence of HIV.

    The loss of CD4 cells from HIV in a healthy person evidently is trivial to non existent – as any sane person would expect. To put it another way, CD4 cells appear to be immune to the deadly influence of HIV, the insidious virus whose mysterious workings are the secret that even Dr Anthony Fauci with all his billions cannot unlock. This study has Gallo on the ropes, backed into a 5% corner. What kind of a paradigm accounts for 5% of the phenomenon it is meant to explain?

    Chris, it is time to jump ship. HIV doesn’t do it. The study authors themselves are telling you that discreetly. The idea that HIV causes AIDS doesn’t do it any more. We have to look for other reasons why people’s immune systems go South. The paradigm is over, Sir! It’s heading for the hard gound at an accelerated rate. Jump, Chris, before it’s too late.

    What is there about these lines that you can’t accept?

    “Other factors, as yet undefined, likely drive CD4 cell losses in HIV infection”

    “The results of our study challenge the concept that CD4 cell depletion in chronic HIV infection is mostly attributable to the direct effects of HIV replication”

    “Future efforts to delineate the relative contribution of other mechanisms will be crucial”

    What is there about the need of Lederman to make the statement you reported he made to Bennett that you don’t see ? “The idea that our findings published today in JAMA can be taken to support the concept that HIV is not the cause of AIDS is ludicrous. The role of HIV as the cause of AIDS has been proven over and over again. Clearly the people who are misrepresenting our work are not only incapable of clear thinking, they are also apparently unable to read.”

    Michael M. Lederman MD

    Get that harness on, Chris. We don’t want to lose you.

  51. trrll Says:

    The results aren’t exactly surprising to anybody who is familiar with individual variation on other medically related measures. For example, blood levels of an anesthetic required to produce unconsciousness can vary as much as tenfold from person to person. Of course, no reasonable person would conclude from that result that anesthetics don’t work.

    The fact is that people vary a lot. We suspect that a lot of that variance is genetic, but in most cases, we don’t actually know. Biology is complicated, and tracking down sources of individual variation can be extremely difficult.

  52. kevin Says:

    For example, blood levels of an anesthetic required to produce unconsciousness can vary as much as tenfold from person to person. Of course, no reasonable person would conclude from that result that anesthetics don’t work.

    Your example is a poor one. We are talking about a specific phenomenen with HIV, namely that HIV causes a depletion of CD4 immune cells leading to increased susceptibility to disease. Whether the effect is direct or somehow indirect, HIV either causes immune cell loss or it does not. This study seems to prove that it does not or that it does not to a degree sufficient to explain AIDS.

    As for your example, well, the mechanism for how anethetics work is not in question. Sure, there are variances in amount needed to sedate different people, but, ultimately, it’s effects are clearly understood. The same cannot be said of HIV. It’s not even close.

  53. Lise Says:

    Kevin,

    Although your reply was definitely spot on, I don’t think you fully appreciate the relevance of Trrll’s analogy.

    What he’s saying is that some CD4+ cells are so strong that it takes ten times the viral load to overpower and kill them. And likewise some people are so resistant that you have to kill their CD4+ cells ten times over before they develop AIDS.

    It’s all quite straight forward really, and it always evens out in the larger statistical picture, so why get all worked up about the details?

  54. trrll Says:

    Your example is a poor one. We are talking about a specific phenomenen with HIV, namely that HIV causes a depletion of CD4 immune cells leading to increased susceptibility to disease. Whether the effect is direct or somehow indirect, HIV either causes immune cell loss or it does not. This study seems to prove that it does not or that it does not to a degree sufficient to explain AIDS.

    Anesthesia is a specific phenomenon. Either an anesthetic drug causes anesthesia or it does not. But that does not mean that one can expect that individuals will not vary greatly in their sensitivity.

    As for your example, well, the mechanism for how anethetics work is not in question. Sure, there are variances in amount needed to sedate different people, but, ultimately, it’s effects are clearly understood. The same cannot be said of HIV. It’s not even close.

    Since when? As a neuroscientist, I can tell you that the mechanism by which anesthetics work is very much in question. But I don’t really see why you think that matters. If the existence of individual variability is grounds to question whether HIV kills T-cells, then it is also grounds to question whether anesthetics work. Logically, the interpretation of evidence cannot be dependent upon whether you think you know the answer.

  55. trrll Says:

    What he’s saying is that some CD4+ cells are so strong that it takes ten times the viral load to overpower and kill them. And likewise some people are so resistant that you have to kill their CD4+ cells ten times over before they develop AIDS.

    And I suppose that you think that some people’s brain cells are so “strong” that you have to anesthetize them “ten times over” before they develop anesthesia.

    Biology is complicated. You generally can’t fit it onto a one dimensional scale of “strong” or “weak”. Even something as seemingly simple as cell death is enormously complicated and affected by a huge number of variables. Death is not merely the failure of cellular metabolism, it is an active cellular response; cells are genetically programmed to die under certain conditions. For example, there are some genes that when damaged cause failure of cell death under specific conditions. Failure of cells to die when they are supposed to is one of the hallmarks of cancer, for example. So it is hardly surprising that there is huge individual variability in the propensity of cells to die in response to a viral stimulus.

  56. German Guest Says:

    Yes, Biology is complicated and it seems we now have a new scientific debate between HIV-Believers and the authors of the JAMA-article (Dr. Benigno Rodríguez et al):

    Predictive Value of Viral Load Testing Questioned:

    “These results, Dr. Rodríguez says, are at odds with current thinking that the rate of CD4 cell loss in a given HIV-positive person can be accurately predicted by his or her viral load.

    In a September 29th Science news article by John Cohen regarding the JAMA report, Dr. Mellors said that he doesn’t buy the conclusion of the study. “We don’t agree with the paper at all,” he was quoted as saying. “[Viral load] is the most powerful predictor of time to AIDS and death.” Dr. Mellors suggested that the JAMA paper’s results may reflect that CD4 measurements vary a great deal in different labs. Dr. Mellors also said that viral loads should continue to play an essential role in determining when to start people on treatment.

    Dr. Rodríguez’s group is sticking to its guns and concludes that CD4 cell loss in HIV-positive people cannot be thought of as a mere consequence of the amount of virus circulating in the blood. These new findings, they say, hint at more complex scenarios of disease progression, and point to the possibility of indirect processes through which HIV can induce damage to the immune system.”

  57. trrll Says:

    Yes, Biology is complicated and it seems we now have a new scientific debate between HIV-Believers and the authors of the JAMA-article (Dr. Benigno Rodríguez et al)

    This is a quite misleading, as the authors of the JAMA article are also “HIV believers.” According to the PI of the JAMA article,

    The idea that our findings published today in JAMA can be taken to support the concept that HIV is not the cause of AIDS is ludicrous. The role of HIV as the cause of AIDS has been proven over and over again. Clearly the people who are misrepresenting our work are not only incapable of clear thinking, they are also apparently unable to read.

    So the scientific debate is not over whether HIV infection is responsible for CD4 cell loss, but over the precise mechanism by which this occurs, and the extent to which HIV RNA levels can be used to predict the course of the disease in a single individual, as opposed to a population. From the article:

    What factors may account for the residual variability in CD4 cell decay rate? HIV infection is associated with heightened T-cell activation and cellular turnover and expression of immune activation markers is associated with both clinical disease progression and rate of CD4 cell depletion. Cellular immune activation is commonly measured through enumeration of the proportion of cells that express markers such as CD38 and HLA-DR by flow cytometry, although this test is not routinely performed in clinical practice. Proposed mechanisms of immune activation–mediated CD4 cell destruction include programmed cell death, bystander cell killing, and accelerated cellular senescence.

    So rather than questioning whether HIV is responsible for the CD4 decline, the authors are questioning the extent to which cell loss is caused by direct killing by HIV, and the extent to which indirect mechanisms such as HIV-triggered immune activation contribute to cell loss.

  58. kevin Says:

    So rather than questioning whether HIV is responsible for the CD4 decline, the authors are questioning the extent to which cell loss is caused by direct killing by HIV, and the extent to which indirect mechanisms such as HIV-triggered immune activation contribute to cell loss.

    It’s comments like this that betray your otherwise astute scientific sensibilities, trrl. One could always salvage the HIV hypothesis, or any other for that matter, by leaving open the possibility of indirect forces as being responsible for a particular phenomenon, in this case immune cell loss; however, most hypothesis are either discarded or suffer major revisions when extensive scientific findings dispute current consensus–in this case, a consensus whose core belief was that HIV was directly responsible for CD4 loss and could thus be used as an accurate predictor of disease progression for all but exceptional cases. This study turns that belief, and all of the HIV dogma that follows, on its head whether the author or his peers agree that it does or not.

    The current climate of HIV-only inquiry should cause any worthy scientist to take pause. When you examine the accummulated data, prima facia, it’s an embarrassment to anyone capable of respecting the sanctity of the scientific method. When you add an examination of the uncensored clinical data to the equation, the current HIV belief system is rather ridiculous.

    Also, your analogy of the workings of anesthesia to the workings of HIV is still a poor one, whether neuroscientist or sandwich artist. Employing such an analogy speaks directly to one the main problems within the HIV community, namely a reverant reliance on unsubstantiated statistical analyses (viral load, CD4 counts, etc) in the face of overwhelming contradictory clinical presentations. Anethesia has been in use since the Classical Age, and they sure didn’t need any surrogate markers to explain the effects of opium.

  59. Lise Says:

    Failure of cells to die when they are supposed to is one of the hallmarks of cancer

    Please bear with me, Dr. Trrll, but I had the impression from this post that the “failure of cells to die when they’re supposed to” now seems to be one of the hallmarks of the HIV=AIDS hypothesis as well. Perhaps I’ve misunderstood?

    If that’s so, I must ask you to excuse me if I stretch your patience further with a silly question. If there are always a “huge number of variables” and causal connections, many of them little understood, to resort to in explaining study results, how would it be possible to falsify the hypothesis “proved over and over again” that just one of those little understood factors, HI Viral load, is the bullet that kills?
    Or is that not what’s claimed to be a straight forward, “proved over and over again” truth?

    And if you’ll bear with me just one more time, since I’m no doubt one of those people Michael Lederman identified as “unable to read”.
    But I just didn’t see where German Guest said that Dr. Rodriguez is not a “believer” in HIV/AIDS. I really must remind my husband to get me a new pair of bifocals – the old doter can afford it on his salary – but it seems to me what German Guest said was that, according to Dr. Rodriguez himself his group’s…

    ” results were at odds with current thinking that the rate of CD4 cell loss in a given HIV-positive person can be accurately predicted by his or her viral load.”

    And it certainly looks that way to me, because Dr. Mellors has replied, as can be seen in German Guest’s post, that

    “We don’t agree with the paper at all. . . [Viral load] is the most powerful predictor of time to AIDS and death.”

    So to my weak eyes and mind, the scientific discussion, as you call it, concerns very specifically the predictive value of viral load.

    All of which brings me back more confused than ever to my first question. Because, you see, Dr. Rodriguez said his results – his results mind you, not his beliefs – are at odds with current thinking.
    But Dr. Mellor doesn’t seem to feel he has to accept any results which may falsify his own beliefs regarding predictive value of viral load. Instead he simply summons, a bit like a deus ex machina if I may say so, one of that “huge number of variables” that so complicates the science of biology:

    “Dr. Mellors suggested that the JAMA paper’s results may reflect that CD4 measurements vary a great deal in different labs”

    It would become too biologically complicated for one of my sex to try to understand inter-laboratory variables as they impact the accuracy of CD4+ cell counts for diagnostic use (at least that’s what my husband says and he’s very much into biology, although not on the human level so to speak)
    But, Dr. Trrll, if you could please just explain to those of us who are “not only incapable of clear thinking, but also apparently unable to read” how any result of a scientific study may falsify “current thinking”, when it’s that easily invalidated?

  60. Dan Says:

    If there are always a “huge number of variables” and causal connections, many of them little understood, to resort to in explaining study results, how would it be possible to falsify the hypothesis “proved over and over again” that just one of those little understood factors, HI Viral load, is the bullet that kills?

    Lise,
    thank you. It sounds like a bit of a conundrum, to say the least.

    You’ve highlighted their “out”.

    It’s a recurring theme with AIDS.

    State emphatically that HIV causes AIDS, but leave yourself an “out”…in most cases it’s simply all the vague language involved…may, possibly, can, might, that are peppered throughout, yet for some reason we’re not supposed to notice as we move boldly forward with the AIDS hypothesis. Other words that get used to describe HIV when the results are incompatible with the dogma are: enigmatic, mysterious, wily, cunning, paradoxical. As a friend of mine wrote on that subject once, said “that’s Latin for bullshit”.

    The biggest “out” though is simply being bold enough to state that time and time again HIV has been proven to be the cause of AIDS, while in the same breath stating that there’s so much that’s not known (which has the added benefit of getting more $$ for research!).

  61. Arthur Gittleman Says:

    HIV is a complex disease. Hopefully this article will push for looking at supplements and herbs. Little money should be given for HIV research in this area. I have done clinical research in FIV and found that supplements can control this disease. From looking at Prednisolone which suppresses overactive expression of virus was able to get an idea of the main determinate for reacting replication of virus which led to other factors in which to create a formula for treating FIV. HIV drugs have been tried on FIV but so far they do not seem to work very long before failing. This is area still being looked at for FIV treatment.

    Viral load test will still be used to see whether HIV drug is failing. Just that it should not be used for other things. This article is helpful to clear up some misconceptions.

  62. Lise Says:

    Thanks Dan.

    Although I must in fairness point out that Kevin got there before me with the same point as afr as I can see.

    And yes I agree, language is always the first that gives them away.

    Somehow people who are into torture seem to have an enemy in language.

  63. trrll Says:

    Please bear with me, Dr. Trrll, but I had the impression from this post that the “failure of cells to die when they’re supposed to” now seems to be one of the hallmarks of the HIV=AIDS hypothesis as well. Perhaps I’ve misunderstood?

    You’ve misunderstood. The point is simply that cell death is a complicated process, affected by multiple biological variables, so there is likely to be a large amount of individual variation even when a clear cause-effect relationship can be shown statistically, just as is the case for many other biological measures, such as drug effects.

    If that’s so, I must ask you to excuse me if I stretch your patience further with a silly question. If there are always a “huge number of variables” and causal connections, many of them little understood, to resort to in explaining study results, how would it be possible to falsify the hypothesis “proved over and over again” that just one of those little understood factors, HI Viral load, is the bullet that kills?
    Or is that not what’s claimed to be a straight forward, “proved over and over again” truth?

    Statistical methods designed to test hypotheses in the presence of individual variation. As others have noted, this sort of individual variation is more the rule than the exception when it comes to disease, so the statistical tools and experimental designs for dealing with it are well established.

    But I just didn’t see where German Guest said that Dr. Rodriguez is not a “believer” in HIV/AIDS.

    By suggesting that there is a scientific debate “scientific debate between HIV-Believers and the authors of the JAMA-article,” he implies that the authors fall into a different category than “HIV-Believers.” Or do you think that he meant a debate between the JAMA authors and themselves? The reality is that the scientific debate is between different groups of “HIV Believers” who favor different hypotheses regarding the predictive value of viral load, while agreeing about the fundamental causal role of HIV in AIDS.

    So to my weak eyes and mind, the scientific discussion, as you call it, concerns very specifically the predictive value of viral load.

    For an individual, yes. But it is important not to confuse predictive value with the question of causality. As Orac points out, referring to yet another example in which causation is clear yet individual predictive value is poor:

    Let’s look at another example: Breast cancer. Let’s look at stage IV disease, which is, in essence, 100% fatal eventually. We actually have pretty good estimates of median survival and what a patient’s chance of living 6, 12, 24, 36, and 60 months after diagnosis are. However, when faced with a single breast cancer patient with stage IV disease, we are pretty poor at predicting how long that particular patient will survive.

    But Dr. Mellor doesn’t seem to feel he has to accept any results which may falsify his own beliefs regarding predictive value of viral load.

    This is still only one paper. No single paper is decisive in science. Results have to be replicated in other laboratories before they become generally accepted. Perhaps Dr. Mellor can show that using better methods of measuring CD4 cells, or by taking other measurable variables into account, it is possible to make stronger predictions based on HIV RNA levels

  64. trrll Says:

    Anethesia has been in use since the Classical Age, and they sure didn’t need any surrogate markers to explain the effects of opium.

    It sounds like you are confused by the distinction between measuring the effects and explaining the effects. Like many other drugs that have been used for ages, the overall effects of opium (which is an analgesic rather than an anesthetic) are known, but many of the effects of opium on the body have not been explained, and there is a huge amount of individual variation in its effects, which is hardly understood at all. Many “surrogate” markers are in fact used for opiate analgesics: binding to specific receptors, levels of intracellular second messengers, activities of various brain centers, particular animal behaviors. But the fact that many of the action of opium still cannot be explained in detail, or that specific individuals often show reactions to opium that cannot be explained in terms of the known mechanisms of action of the drug, is not a valid reason for disputing the classification of opiates as an analgesic drugs.

  65. MacDonald Says:

    so there is likely to be a large amount of individual variation even when a clear cause-effect relationship can be shown statistically

    Dr. Trrll, I for one begin to see now. Cause-effect relationships are shown statistically ermm. . . So how was it again a cause-effect relationship differed from mere correlation?

    This is still only one paper. No single paper is decisive in science

    Yes that’s clear and consistent to any reasonable person. If no single patient is anything but a dismissable part of a statistic, how can any single scientific paper be?

    It’s all clear as stats to me now how the hypothesis, HIV causes AIDS , is ‘proved over and over again’. One simply takes all the papers published on the subject, ignores all the ‘inter-individual variation’, all the little puzzles and discords, runs a statistical analysis of their stated conclusions, and Bob’s your uncle.

    Amazing.

  66. kevin Says:

    This is still only one paper. No single paper is decisive in science. Results have to be replicated in other laboratories before they become generally accepted.

    Where was this handy rule back in 1984?

    Gallo’s findings were universally accepted before being proven through the peer review process. Sure the Frenchies were studying HTLV-1 and cancer…hell, that’s where Gallo first found “the virus that causes AIDS”, but they did not present a paper asserting that HIV=AIDS. Gallo’s work was accepted without question due to the political nature of the research and the social hysteria associated with AIDS. Now the “virus that causes AIDS” has become “the virus that causes immune cell loss, in some as yet to be identified way”. Too bad, that won’t fit on a bumper sticker.

  67. Arthur Gittleman Says:

    My interpretion of article is that using NRTI, NNRTI and PI is really only covers 10% of decrease and that there is a need to find drugs that will cover the missing 90% in order to improve HIV treatment. This points to the future. 90% of CD4 cell depletion remains enigmatic. I really don’t think it is that enigmatic. Most of the depletion is caused by overactivating of T-cells. Part of the 90% will be inhibiting entry of virus into cells. And that is being developed presently. The is also the problem of CD4 cells dying that should not happen as they are not infected by virus. The article concluded with, “The results of our study challenge the concept that CD4 cell depletion in chronic HIV infection is mostly attributable to the direct effects of HIV replication. Future efforts to delineate the relative contribution of other mechanisms will be crucial to the understanding of HIV immunopathogenesis and to the ability to attenuate it.”

    There have been questions on when to start HIV treatment which was based on previous study done in 1996 on viral load. This study being into question these standards. Last I heard viral load of 30,000 was break point with count of 350 or 200 CD4. Don’t know what the latest standard is. But you can see what problem this article brings up. Of cause, doctors don’t really follow this. But this is what I keep reading as the standard, so now expect of new theory on when to start treatment. That is for HIV. For FIV this would be nonsense as one does not what to treat a disease normally. Because current HIV drugs are so toxic you wonder when to use them. Worse is that many people the have HIV to not want to take them. Which bring use back to what about this 90 percent?
    I should mention that fact if patient has low Cd4 count he may not progress to AIDS if his Interferon-alfa is high. This is for people who think you get AIDS from low CD4 count. ….Not all the time.

  68. kevin Says:

    It sounds like you are confused by the distinction between measuring the effects and explaining the effects.

    No, I’m not confused in the least about the difference. I’m simply asserting that your analogy was BS. There is a greater burden of proof in establishing the effects, whether measurable or not, of a discovered pathogen (HIV) as opposed to measuring the effects of a discovered remedy (anesthetics). The remedy is often discovered precisely because its effects are apparent and
    beneficial . Thus, it’s easier to test the cause and effect connection of a remedy and its suspected effects–less risk. The pathogen, on the other hand, endures a similar discovery in that it is first suspected to exist precisely because of its effects, undesirable effects, mind you. However, these undesireable effects do not necessitate the existence of the pathogen. Also, the connection between the effects and the pathogen is certainly not apparent. That must be proven, and HIV has failed to be proven as the pathogen that causes this illness, assuming there is one. My understanding is that lots of scientists have had theories as to the “how” but the ultimate explanation has suffered radical changes over the years–paradigm-killing changes, I’d say. However, if it has been proven, Dr. Trrl, please enlighten me as to paper that contains the conclusive evidence of how HIV causes this illness. Or even, which explanation (cite paper again, if possible) do you think holds the most water?

    Furthermore, before we can measure the effects of HIV on living people, it should be necessary to isolate the virus directly from the human body and not from a petri dish concoction. Once we are measuring quantities of actual HIV from a human’s blood sample and not merely amplified DNA markers, then I’ll admit that progress has been made. After all these years of obfuscation, I’m not holding my breath, but I’m far from confused.

  69. trrll Says:

    Cause-effect relationships are shown statistically ermm. . . So how was it again a cause-effect relationship differed from mere correlation?

    Cause-effect is distinguished from correlation by
    a) Prospective studies, in which the health of people is followed after they become infected with HIV
    b) Intervention studies, such as studies of the health of people treated with drugs directed against the HIV virus
    c) Animal studies of experimental infection with related viruses
    d) In vitro studies examining the effects of the virus on cells.

    One simply takes all the papers published on the subject, ignores all the ‘inter-individual variation’, all the little puzzles and discords, runs a statistical analysis of their stated conclusions, and Bob’s your uncle.

    Yes, this is basically a description of the science of epidemiology, and is the basis of most of what we know about disease and the effects of drugs and other substances on the body. Fundamentally, it is the science of seeing the forest through the trees, and separating general truths from the confusion of individual diversity. That is not to say that individual variation is not important, but it frequently reflects different processes, so it is an error to imagine that if you cannot explain “all the little puzzles and discords,” then you cannot draw any valid conclusions.

  70. Michael Says:

    Dear Arthur. You said: 90% of CD4 cell depletion remains enigmatic. Not if you consider that 90% of illness has unmeasureable emotional and mental factors, and with a diagnosis of HIV or AIDS, this includes extreme and extensive feelings of shame, guilt, fear, and hopelessness.

    Of course, those who have had more sheltered lives may never have noticed the negative effects that regular immersion in these emergency and crisis emotions have on health, and many people are generally fairly clueless as to their impact on health and illness.

    Unfortunately, science is not able to measure death wishes or measure the manifestation of the negative thinking and emotional factors that go along with being told “YOU HAVE HIV, The virus that causes AIDS”, as the poor fool then needs to be carried out of the building and into a suicide watch!

  71. trrll Says:

    There is a greater burden of proof in establishing the effects, whether measurable or not, of a discovered pathogen (HIV) as opposed to measuring the effects of a discovered remedy (anesthetics). The remedy is often discovered precisely because its effects are apparent and
    beneficial. Thus, it’s easier to test the cause and effect connection of a remedy and its suspected effects—less risk.

    I think this reflects a severe lack of knowledge about how difficult it is to identify the effects of putative “remedies.” In fact, almost all drugs produce a complex mixture of desirable and undesirable effects, obscured by a high degree of individual variation. There are many examples of cases where a drug was imagined to be beneficial until detailed statistical studies showed that in fact it was doing more harm than good. But of course, the question is not one regarding “burden of proof,” but rather what level of individual variation one should expect in biological phenomena. And study after study shows that individual variation is likely to be large, both for pharmacological effects and disease processes.

    My understanding is that lots of scientists have had theories as to the “how” but the ultimate explanation has suffered radical changes over the years—paradigm-killing changes, I’d say. However, if it has been proven, Dr. Trrl, please enlighten me as to paper that contains the conclusive evidence of how HIV causes this illness.

    In fact, the question of exactly “how” a particular disease causes all of its symptoms is one that can rarely be answered definitively for any illness. Identifying a causative agent is much easier than identifying mechanisms. The original hypothesis that HIV produces its effects by depleting immune cells seems to have held up remarkably well (and is supported by the correlation in this paper). But the exact details of how that comes about will probably take many more years to work out.

  72. trrll Says:

    Gallo’s findings were universally accepted before being proven through the peer review process. Sure the Frenchies were studying HTLV-1 and cancer…hell, that’s where Gallo first found “the virus that causes AIDS”, but they did not present a paper asserting that HIV=AIDS. Gallo’s work was accepted without question due to the political nature of the research and the social hysteria associated with AIDS. Now the “virus that causes AIDS” has become “the virus that causes immune cell loss, in some as yet to be identified way”. Too bad, that won’t fit on a bumper sticker.

    Gallo’s results were considered quite impressive at the time, but that didn’t stop scientists from doing further studies to test the predictions of Gallo’s theory. Today, a MedLine search for “HIV” and “AIDS” yields over a hundred thousand references. The modern understanding of the relationship between HIV and AIDS rests less upon Gallo’s work than upon the thousands of publications that followed up on that work.

    And by the way, peer review does not “prove” anything. It provides basic quality control and catches some errors. But plenty of peer-reviewed papers fail to pass the much stronger test of independent experimental confirmation.

  73. Truthseeker Says:

    Gallo’s results were considered quite impressive at the time, but that didn’t stop scientists from doing further studies to test the predictions of Gallo’s theory. Today, a MedLine search for “HIV” and “AIDS” yields over a hundred thousand references. The modern understanding of the relationship between HIV and AIDS rests less upon Gallo’s work than upon the thousands of publications that followed up on that work.

    This is an absurd statement, first, in terms of fact. Gallo’s results were not considered impressive by any informed person at the time, even by himself, and it was only the political enthusiasm of Margaret Heckler that resulted in the press conference making the claim oficial before anyone had reviewed the papers. No one was more surprised by the rapidity of events than Gallo, though it didn’t stop him nailing down the patent by the end of the day.

    Secondly, in terms of reason. The fact that Medline shows hundreds of thousands of references for HIV and AIDS means absolutely nothing in terms of “testing the predictions of Gallo’s theory”. All the papers assume that his claim was correct; none of them question it; all of them use it as an unquestioned premise.

    That is the corruption that runs through HIV∫AIDS and vitiates any idea that the sheer numbers of papers validate Gallo. To talk of the “modern understanding of the relationship between HIV and AIDS” as if there was any understanding of any kind, and that there was not a constant stream of papers revealing this total lack of understanding, including the one under discussion in this post, and a constant mainstream high level discussion of this lack of understanding, and a constant reference to this lack of understanding as a “conundrum” etc, is to show no familiarity at all with even a sprinkling of the relevant papers on the topic.

    It is this kind of announcement of unexamined faith in beliefs that are essentially concocted by the speaker and not even checked against the literature that makes the task of this blog so difficult. There is not one prediction of the Gallo theory that has been realized, as far as we know. Perhaps you would like to name one. In fact, it is the predictions of the dissenters that all have been realized, as Duesberg has demonstrated.

  74. Arthur Gittleman Says:

    Dear Michael, you bring up a good point. Emotional and mental factors are a big part of problem in this disease. Most articles do not cover this problem as drug companies see no profit to be made. I see this problem in the HIV boards and blogs. Doctors are not normally trained in this area. Perhaps it is subject that is not talked about. It is a fact that HIV attacks the brain and this is a problem. Most people with HIV should be taking Niaciamide as the disease reduces this which can cause depression. I guess you can call this part of the 90 percent that is ignored. Some of these cheap or little cost things are ignored and only high profits drugs are given space in most studies. In using Niaciamide my FIV cat went from 2,000 lyumph count to 3,000 as it is also an FIV or HIV inhibitor. It acts similar to intergrase inhibitor. Some people assume that the only things that work are your HIV drugs that bring in big profits for drugs companies. This is one of the problems in the current HIV field as cheap things are not given any humans tests. I see this with Bovine Lactoferrin which inhibits DC-Sign.

    It is interesting that when you fail HIV drugs the HIV virus has been weakened to 1/3 of its strength. At that point one can use drugs or herbs that do not have as great of inhibiting factor as the normal HIV drugs. Yet you are not going to see this as this would reduce the drug companies profits. I have noted drug companies purchasing patents and suppressing them in order not to compete with there latest drug they have on the market. Drug companies are in the business to make profits and that may be in comflict with best interests of HIV patients. The study of emotional and mental factors are given little funding as this is not where the big money is to be made.

  75. noreen martin Says:

    Mr. Gittleman, you have touched on a very important part of this disease. It’s an emotional roller-coaster ride from hell. Not only is one dealing with the stigma of being HIV+ or having AIDS, then factor in the “incurable” aspect of the situiation along with the toxic drugs which one is highly pressured to comply with or else there is another emotional issue to deal. It’s a mind game all the way around. This is the negative side of AIDS. I would recommend that anyone who have to deal with this to seek counseling, talk to others in the same boat, use the internet or what ever means that works, as one must have the right mental attitude, regardless of how one stands on the issue, to effectively beat this and survive.

  76. trrll Says:

    Secondly, in terms of reason. The fact that Medline shows hundreds of thousands of references for HIV and AIDS means absolutely nothing in terms of “testing the predictions of Gallo’s theory”. All the papers assume that his claim was correct; none of them question it; all of them use it as an unquestioned premise.

    The fact that a paper does not emphasize that it is testing the HIV/AIDS relationship does not mean that it is not a test. When a scientist writes up his work, he is going to present it in as interesting a way as possible. Coming up with additional data to confirm an already widely-accepted hypothesis is not news, so a scientist will emphasize this aspect of his results only if they are in disagreement with the generally accepted view. Of course, every scientist would love to do the experiment that overturns the generally accepted paradigm, but you have to have a secondary goal in case you are unfortunate enough to get results that are in agreement with what is already widely believed.

    For example it is not news that on a population basis, HIV levels go up as CD4+ cell go down, although it certainly would be a problem for the theory if they did not. It is worth noting that in his early papers, Duesberg argued that the development of disease years after infection was inconsistent with HIV as a causative agent because HIV was already “neutralized” by antibodies. If subsequent studies using more sensitive PCR based assays had supported Duesberg’s contention, rather than revealing that virus was increasing during the so-called “latent” period, then scientific opinion would have doubtless shifted in Duesberg’s favor.

  77. kevin Says:

    But of course, the question is not one regarding “burden of proof,” but rather what level of individual variation one should expect in biological phenomena. And study after study shows that individual variation is likely to be large, both for pharmacological effects and disease processes.

    I don’t disagree with your explanation regarding importance of understanding individual variation in assessing the efficacy of a particular remedy or drug. However, I still contend that your original analogy was fundamentally misleading, in the same way that so much of what comes from the HIV/AIDS megaphone is i.e. comparing the indivual variations of sensitivity to anesthetics to the current discussion regarding the usefulness of viral load in predicting CD4 loss is ridiculous. There are fundamental questions regarding the integrity of viral load data that need to be answered before such an analogy is not so insulting.

    And by the way, peer review does not “prove” anything. It provides basic quality control and catches some errors. But plenty of peer-reviewed papers fail to pass the much stronger test of independent experimental confirmation.

    Or some are never put to the test of independent experimental confirmation, as Truthseeker has explained. See Dr. Gallo’s discovery of “the virus the causes AIDS” for an example of a theory that has been “proven” by peer-review alone.

    Alas, if only all HIV medical professionals and research endeavors were as pure and rigid as you are, Dr. Trrl.

  78. kevin Says:

    There are many examples of cases where a drug was imagined to be beneficial until detailed statistical studies showed that in fact it was doing more harm than good.

    The opposite is also true: cases were a drug has not been tested for a particular benefit, yet doctors prescribe it “off-label” because of its obvious clinical benefits. Of course, that requires a doctor who is capable of critical thinking and one who respects a patient’s ability to assess his/her own well-being as part of a quality doctor/patient relationship. I haven’t met a doctor yet who knows more about my body than I do, but I’ve met plenty who are sure that they do, even without learning of my health history–all because they’ve mastered the liturgy of PharmaUSA.

  79. MacDonald Says:

    Dr. Trrll,

    I guess this is one of the many, many exceptions that confirms every causal relationship.

    Likewise it’s one of those cases that confirms researchers don’t always, always go for the BIG HEADLINE, although really, really they alaways, always set out to test the hypothesis that viral load corresponds with CD4 cell decline.

    However, within each viral load group the investigators observed a large interpatient variability of individual CD4 loss. This was true across all of the different viral load strata, and included individuals who gained CD4 cells

    I guess in this case they didn’t want the publicity either cuz they know that, statistically speaking, this observation is wrong.

  80. Chris Noble Says:

    This is an absurd statement, first, in terms of fact. Gallo’s results were not considered impressive by any informed person at the time, even by himself, and it was only the political enthusiasm of Margaret Heckler that resulted in the press conference making the claim oficial before anyone had reviewed the papers.

    Gallo’s papers had been submitted to Science, had gone out to scientific reviwers, had passed review, had been deemed impressive and worthy of publication and had been accepted for publication before the press conference.

    Check the acceptance date on the papers if you want.

  81. Michael Says:

    Dr. Gittelman. Thank you for your mention of Niacimide. From my own perspective, your experience with this Niacin derivative further shows that disease presumed to be due to HIV or even FIV has more to do with nutrition, toxins, and other factors than any supposedly destructive retroviral activity.

    You made a statement of your belief that I found to be highly questionable. You said: It is a fact that HIV attacks the brain and this is a problem.

    I don’t find any studies whatsoever that prove HIV doing anything whatsoever in the brain tissues and cells, that could not just as easily have been due to other factors. I do, however, find that many of the people said to have brain damage blamed on HIV, are in fact people who have either abused recreational drugs in extreme, or, I also find that many of the HIV drugs, especially the most toxic chemotherapeutic ones, do indeed pass the blood/brain barrier. The cellular damage due to most all of these potent HIV drugs is extensively proven, especially AZT, which has repeatedly shown brain damage and brain lesions caused by it. Unfortunately, I think, many researchers jumped to a premature conclusion that HIV was at the center of brain disfunction, but this has not yet been proven to be true sir, only presumed to be true.

    The blood-brain barrier prevents many antiretroviral drugs from passing into the brain. However, the drugs which do demonstrate consistent penetration into the CerebroSpinal Fluid are AZT, d4T (stavudine, Zerit), 3TC, nevirapine, efavirenz (Sustiva) and indinavir, although there seems to be considerable interpatient variability (Wynn 2002). There are few comparative data on the concentrations reached by different drugs in the CSF.

    A study of 63 consecutive highly active antiretroviral therapy (HAART) patients who underwent lumbar puncture at a Rome hospital found that nevirapine, indinavir, d4T and 3TC were present at the highest concentrations in the CerebroSpinal Fluid, with undetectable CSF concentrations of ddI, efavirenz and nelfinavir (Viracept; Antinori 2002). The ratio of drug in the CSF compared to the plasma ranged from 0.02 for AZT (normally thought to have the best penetration) to 0.6 for nevirapine.

    Also, Dr. Gittelman, although I understand your own beliefs to be that FIV is the causal agent of immune dysfunction in cats, I also find this to be questionable as well. Before deciding for yourself that I am unquestionably wrong on this issue, I recommend that you read Dr. Harvey Bialy’s book, “Oncogenes, Aneuploidy, and AIDS”, especially page 173, for a clearer understanding of how the science of FIV came to be in the first place. You yourself may conclude that all is not well with calling any retrovirus the cause of any disease.

  82. Chris Noble Says:

    Chris, for the benefit of onlookers one can only repeat that you are contradicting the study authors, who are explicitly perplexed by the little association they found between CD4 cell count and HIV viral load.

    You are the one that is contradicting the study authors.

    The study shows that there is a definite and significant relationship between HIV viral load and the rate of CD4+ cell depletion at the population level. The relationship is there. You can deny it all you want but it is still there. Denying the experimental evidence makes you a “denialist” rather than a “rethinker”.

    Not one of you can come up with a plausible explanation for the relationship between HIV viral load and CD4+ cell depletion.

    All you do is deliberately misrepresent this study.

    Even one of the authors has come out to state that your position is a misrepresentation.

  83. Michael Says:

    Chris, you said:

    Gallo’s papers had been submitted to Science, had gone out to scientific reviwers, had passed review, had been deemed impressive and worthy of publication and had been accepted for publication before the press conference.

    Chris, Pleeeease share with us the name of any of the reviewers that had any background whatsoever in retrovirally caused disease, or even in any retroviruses at all, and then we can decide just how impressed and impressive any of these claims were.

    The fact is Chris, none of your so-called reviewers had any knowledge in the science of retroviruses or retroviral diseases whatsoever, and no disease had ever before Gallo’s claims of HTLV-III, had ever been proven to be caused by any retrovirus! I am sure they were mighty impressed by it, as it was something that absolutely none of the reviewers even had any knowledge of or experience in. But SCIENCE Magazine certainly had Gallo beating on them to quickly get it printed before someone else, like, Luc Montagnier, might make any claims on something such as LAV being the cause of AIDS. Your display of fawning over someone such as Robert Gallo, whom was proven to have mis-appropriated LAV and called it HTLV-III, as well as having been proven to have manipulated his own lab guys findings, as well as having been proven to have mis-appropriated the T-cell culture he cultured it in and that he falsely claimed as his own, is really a bit much.

    Impressed? Not!!!

  84. Bialyzebub Says:

    I think I have never encountered a more totally ignorant of any facts whatsoever and so totally embedded in their own going to seed and fat and miserable, useless insignificant lives who even comes close to Noble.

    He appears, like Bush and Clinton and others that TS admires, a total idiot, who actually knows nothing about the way science really works, and is woefully ignorant of any of the historical literature that day by day almost depicts the way the AIDS virus was created, and much of it is availabale on the internet, his favorite, perhaps only research tool. Nothing, less even than Undergrad. Gal/Guy.

    Get it?

    There are flies all over your fat and very empty head.

    How’s that for “spewing ad hominal abuse”?

  85. Chris Noble Says:

    The fact is Chris, none of your so-called reviewers had any knowledge in the science of retroviruses or retroviral diseases whatsoever, and no disease had ever before Gallo’s claims of HTLV-III, had ever been proven to be caused by any retrovirus!

    Have you actually looked at the paper’s that were published before 1984 regarding diseases caused by retroviruses?

    Your revision of history is atrocious.

  86. Lise Says:

    Not one of you can come up with a plausible explanation for the relationship between HIV viral load and CD4+ cell depletion.

    Dr. CNN,

    all your waffle doesn’t in the least distract anybody from the fact that you can’t come up with a plausible explanation for the relationship between yellow fingers and HIV infection.

    You haven’t even explained why cell free HIV is knobless, although my husband assures me that’s your field of expertise.

  87. Chris Noble Says:

    How’s that for “spewing ad hominal abuse”?

    Top marks.

    Now what is your explanation for figure 1 in the recent JAMA article that is supposedly the subject of this thread?

    Why is there any relationship whatsoever between HIV viral load and the rate of CD4+ cell depletion in HIV infected people?

    Simple question.

  88. Bialyzebub Says:

    Moron,

    Read this, and learn something.

    It was a top ten on Rockwell for 4 days, which means that more than 10,000 people with IQ’s higher than yours read it and found it informative.

    Argue with the author if you wish. It ain’t me.

  89. Mia Lancaster Says:

    How astute is Dr. Gittleman’s reference to FIV and his belief that disease presumed to be due to FIV (or HIV) has more to do with nutrition, toxins, and other factors than destructive retroviral activity.

    Anyone who cares about cats as living beings who deserve as much care from humans as they need to live contented lives should know that there has been a similar tendency to sacrifice cats’ lives to medical beliefs which many people think are fantasy.

    I have been deeply involved in cat rescue and adoption for nearly 20 years, from 1987 to the present. In 1990, I founded a not-for-profit organization and have remained director since then, overseeing the care of approximately 200 or more cats per year. Very early in my work, I publicly opposed the killing of strays merely because they tested positive for what was called feline aids (FIV) virus and/or for feline leukemia (FeLV) virus.

    In the late 1980s and early 1990s, I witnessed with horror people in vet’s offices tearfully euthenizing a kitten or a cat even though the animal appeared healthy, playful, and without any signs whatsoever of an illness except that the blood test had come back positive.

    Few people realize that even more than veterinarians, shelter directors (who usually are not veterinarians,) nonetheless have far more hands-on practical, daily experience in recognizing cat symptoms and treating cat ailments. By the mid-1990’s it became known among shelter directors that most of the time, both FIV and FeLV passed through the system of the cat, once the stray was placed into a healthy environment, given good food, TLC, and basic medical care (worming, removal of fleas, ticks, ear mites, etc., if any, and vaccinated against distemper). The positive blood test was revealing raised antibody level due to the correct, healthy response of the feline’s body to having been subjected to a virus. It did not mean that the animal had acquired the virus.

    However, veterinarians continued to recommend to caregivers that cats who blood-tested positive, but who exhibited no ill symptoms, be killed. This disgusting practice made no logical sense to me. It became even more difficult to remain objective in finding homes for cats, since it became equally clear that the lay person (adopter) was inclined to disregard a shelter director’s information in favor of a veterinarian’s recommendation, even if the recommendation meant murder of a cat. Having superior hands-on knowledge of the course of cat virus (to cat recovery) made it difficult to continue my work.

    In other words, according to the then-treatment, if cats were people, any person appearing with a flu virus should be killed, not treated.

    Finally, by the late 1990s, it became common veterinary knowledge that automatically re-testing a kitten or a cat about 2 months after the animal’s initial blood test came back positive almost always returned a negative blood result for the virus. Finally, the summary murder of healthy cats and kittens whose systems were correctly working in the first place ceased.

    If good food, good hygiene, personal care and basic medical attention worked for FIV-positive cats, it should work for HIV-positive humans.

    In addition, my nutritionist, who is on the advisory board of Life Extension, Carmen Fusco, R.N., told me back in 1990 that nutritional supplements such as Immuplex work miracles for anyone dealing with a lowered immune system (lowered for any reason including her patients diagnosed with AIDS.)

    I never understood why harmful pharmaceuticals were imposed on the HIV-positive individuals when benign nutritional remedies were available.

  90. Chris Noble Says:

    Moron,

    Read this, and learn something.

    Still no answer regarding figure 1 in the JAMA paper.

  91. Chris Noble Says:

    all your waffle doesn’t in the least distract anybody from the fact that you can’t come up with a plausible explanation for the relationship between yellow fingers and HIV infection.

    Are you claiming that yellow fingers is predictive of HIV infection?

    If you are claiming that yellow fingers and risk of HIV infection are in any way correlated then the plausible reason is that a third factor – smoking tobacco causes a) yellow fingers and b) a higher risk of many infections possibly including HIV.

    If the relationship between HIV viral load and the rate of CD4+ cell depletion is not causal then could you come up with a third factor that explains the correlation?

  92. trrll Says:

    I don’t find any studies whatsoever that prove HIV doing anything whatsoever in the brain tissues and cells

    You must not have looked very hard, then. A simple Medline search for “HIV neurotoxitity” (the most obvious search I could think of) turns up hundreds of studies, including quite a few studies showing HIV doing a variety of things (most of them not good) to brain tissues and cells.

  93. trrll Says:

    I guess in this case they didn’t want the publicity either cuz they know that, statistically speaking, this observation is wrong.

    An observation of a particular individual cannot be wrong, “statistically speaking.” It can at most be said to be uncommon.

  94. trrll Says:

    There are fundamental questions regarding the integrity of viral load data that need to be answered before such an analogy is not so insulting.

    No analogy is being made. Rather, it is a point of logic. If interpretation of a particular piece of data depends upon what you think the conclusion is, it is rationalization, nor rationality. If high individual variation is evidence against a causal relationship in one context, it must indicate the same thing in other contexts.

  95. Lise Says:

    If you are claiming that yellow fingers and risk of HIV infection are in any way correlated then the plausible reason is that a third factor – smoking tobacco causes a) yellow fingers and b) a higher risk of many infections possibly including HIV.

    If the relationship between HIV viral load and the rate of CD4+ cell depletion is not causal then could you come up with a third factor that explains the correlation?

    Dear Dr. CNN,

    How about tobacco smoking?

    Really now, how many times do I have to encourage you to develop some confidence in yourself and start trusting your own perfectly good answers instead of boring everybody to death by asking these incredibly silly questions over and over? It’s no way for a grown man to behave.

  96. Chris Noble Says:

    How about tobacco smoking?

    I was asking for a plausible explanation.

    Are you really trying to argue that smoking tobacco cause a) the selective depletion of CD4+ cells and b) the dramatic increase in a virus that infects these cells?

    By the way the study that you referred to regarding the possible relationship between smoking and risk of HIV infection found no significant relationship between smoking and progression to AIDS.

  97. Truthseeker Says:

    How’s that for “spewing ad hominal abuse”?

    Not strong enough. Not nearly strong enough. Far too genteel, in fact.
    Dr Beelzebub, the quality of this blog now depends on the willingness of yourself and other critics here to verbally hang, draw and quarter those that clog up Comments with repeated stupidities.

    NAR Change in Policy statement:

    The policy of this blog is now changed from the previous tolerance for blind foolishness and maintenance of the highest club standards of collegial civility for all comers, on the false assumption that all were truthseekers prepared to examine the evidence on its merits and use their brains to assess its meaning, in a spirit of cooperation and dedicated scientific endeavor.

    Unfortunately, it appears that this policy allows free rein to people who have neither the wit nor the will to understand replies to their requests for enlightenment and whose repeated return to points that have already been dispensed with in six different ways becomes both irritating and time wasting, not to mention liable to mislead onlookers, especially since the posted comments are self-evidently aimed more at gaining attention to the writer rather than any honest quest for enlightenment.

    In recognition of the many who have suffered excruciating agony and death at the hands of those who have blocked genuine review of this paradigm, from now on all posts aimed at such fellow traveling dolts which are wittily and severely corrective will automatically gain a green border regardless of ad hominem terminology.

    In other words, wilful stupidity will no longer be tolerated on this site and open season is now declared on those guilty of it.

  98. Lise Says:

    I guess in this case they didn’t want the publicity either cuz they know that, statistically speaking, this observation is wrong.

    An observation of a particular individual cannot be wrong, “statistically speaking.” It can at most be said to be uncommon

    Reduced to rather small steps now aren’t we, Dr. Trrll? But ok:

    I guess in this case they didn’t want the publicity either cuz they know that, statistically speaking, this observation is uncommon ?

    Feel free to answer both of the original questions now, unless of course there’s a misplaced comma somewhere that needs to get sorted in its own private post.

    While you’re at it, are you absolutely sure that you want your name forever associated with this definition of the criteria of falsification in the case in question, which, if you care to remember, was that ANY statistical “anomaly”, can be explained (away) by “the huge number of variables” in the science of biology?

    Statistical methods designed to test hypotheses in the presence of individual variation .

    Perhaps you could tell us exactly how that would work in the present case.

  99. Arthur Gittleman Says:

    Dear Michael, my only experience has been the use of Vital Pet which contains procaine in dealing with FIV neuro problems caused by the disease. For some reason amyloid deposits are created by the disease. Vital Pet is similar to GH3 which has been used as an MOI inhibitor. Its history goes back to 1944. HIV drugs to not cover the problem of depression caused by the virus. And most likely depression caused by the virus is not treated by some HIV doctors. I have used Vital Pet on my FIV cat and seen positive results. I should mention that this is similar to Anticort which is now called SPo1A a HIV drug which is in phaseIII testing in Europe. Amyloid tissue deposits are contained in many diseases.

  100. trrll Says:

    I guess in this case they didn’t want the publicity either cuz they know that, statistically speaking, this observation is uncommon?

    If they were inclined to make an issue of a rise in CD4+ levels in a few individual patients, they probably would have been required to delete it by peer reviewers, who would have correctly pointed out that it is a well-known statistical error to select out particular individuals at one extreme or the other of the distribution and try to draw conclusions based on the fact that they are at an extreme.

    While you’re at it, are you absolutely sure that you want your name forever associated with this definition of the criteria of falsification in the case in question, which, if you care to remember, was that ANY statistical “anomaly”, can be explained (away) by “the huge number of variables” in the science of biology?

    Not really. It would be hard to explain if the average viral level did not correlate with the average CD4+ level. As I said before, if this had not turned out to be true, scientists would doubtless have given more credence to Duesberg’s argument that HIV was effectively “neutralized” by the immune system and thus incapable of doing harm. Anecdotal observations of specific individuals are rarely scientifically informative, aside from telling you that there are additional uncontrolled variables—which is so routinely the case in studies of disease or drug effects that it is not particularly remarkable. In a particularly clear case, it might be useful to study outlier individuals to determine what makes them different from average, but this is risky, because there is no guarantee that the particular individual’s deviation from the mean will be the result of a single clear factor. It could just as well be a combination of numerous factors with individually small effects that all happened to stack up in the same direction at that particular moment in time when the measurement was taken: A change in diet, exposure to environmental allergens, exposure to environmental chemicals, medications take for other conditions, life events that affect the patient’s emotional status, differences in genetic makeup, etc., etc. If this is the case, it will almost certainly not be possible to disentangle which influences are significant and which are not. This is why scientists generally prefer to study populations, where statistical analysis allows reliable, reproducible conclusions to be drawn even if there is unexplained individual variation.

  101. Lise Says:

    Dr. Trrll,

    Thank you for that answer – finally.

    I’ll let those few who’ve made it this far read it and decide for themselves how and when correlation turns into causation in HIV Science. Likewise those who wish to do so can now determine whether the HIV/AIDS hypotheses passes the test of falsifiability.

  102. Dan Says:

    Another cheer for Lise!

    Brilliant!

    The HIV=AIDS hypothesis is nothing but correlation!

  103. nohivmeds Says:

    Michael wrote:

    “Unfortunately, science is not able to measure death wishes or measure the manifestation of the negative thinking and emotional factors that go along with being told “YOU HAVE HIV, The virus that causes AIDS””

    In fact, Michael, all of these things can be measured. The field that measures these things is called psychology, as I’m sure you’re aware. Your hypothesis that psychological factors contribute to AIDS is testable, and I agree with the hypothesis. You should advocate, as I do, for more behaviorally/psychologically-based research in this area.

  104. nohivmeds Says:

    To be more specific, the subspecialty you are looking for is PNI, or Psychoneuroimmunology. Not a new field at all, but one that is producing very exciting results regarding the impact of psychological states on physical health. For example, depression (for which there are many measures) is significantly correlated with a decline in NK cells, and therefore, a deficit in cellular immunity. “Death wishes” or suicidal ideation, has also been correlated with decreases in immune function.

  105. Gene Semon Says:

    “Future efforts to delineate the relative contribution of other mechanisms will be crucial to the understanding of HIV immunopathogenesis and to the ability to attenuate it.”

    How about one from the past?

    “Clinical studies presented here directly demonstrate that low GSH (glutathione) levels predict poor survival in otherwise indistinguishable HIV-infected subjects. Specifically, we show that GSH deficiency in CD4 T cells from such subjects is associated with markedly decreased survival 2-3 years after baseline data collection (Kaplan-Meier and logistic regression analyses, P < 0.0001 for both analyses). This finding, supported by evidence demonstrating that oral administration of the GSH prodrug N-acetylcysteine replenishes GSH in these subjects and suggesting that N-acetylcysteine administration can improve their survival, establishes GSH deficiency as a key determinant of survival in HIV disease.

    “GSH deficiency has long been known to be clinically dangerous in man and in experimental animals. T cell function and viability are markedly impaired in GSH-depleted T cells.” (Herzenberg et al, PNAS, Vol. 94, pp. 1967-1972, March 1997)

    I would enjoy a response from trrll.

  106. MacDonald Says:

    Dr. Semon (I know you are)

    We all enjoy Trrll’s responses, man and his experimental animals alike.

  107. nohivmeds Says:

    Dearest Chris Noble, who wrote:

    “The study shows that there is a definite and significant relationship between HIV viral load and the rate of CD4+ cell depletion at the population level. The relationship is there. You can deny it all you want but it is still there. Denying the experimental evidence makes you a “denialist” rather than a “rethinker”. ”

    There is also a significant relationship between exposure to radiation and CD4 cell depletion, exposure to environmental toxins and CD4 cell depletion, excessive drug use and CD4 cell depletion, etc., etc., etc. All the correlations in the world don’t “prove” that HIV is causing the CD4 cell depletion seen in this study. Were all other variables that could cause CD4 cell depletion controlled for? No, they weren’t. Does correlation equal causation? Nope, it doesn’t.

  108. nohivmeds Says:

    There could be (may actually be) 200,000 papers showing a correlation between CD4 cell depletion and viral load — it’s all irrelevant without the causal mechanism, which is unknown, at least according to Zvi Grossman. Gimme a call when Dr. Grossman says we know what the causal mechanism is. In the meantime — you can drown me in correlations if you’d like, but you still will not have proven that which you are so desperate to prove — that HIV infection causes AIDS. That requires a clear understanding of HIV pathogenesis, and that does not exist after 25 years of research. Even another 200,000 correlations will still be unimpressive, dearest Chris Noble. Causal mechanism, my friend — that’s all that counts.

  109. Robert Houston Says:

    Chris Noble has reiterated several versions of following question:

    “If the relationship between HIV viral load and the rate of CD4+ cell depletion is not causal then could you come up with a third factor that explains the correlation?”

    In fact, there are several third factors, which appear to be interrelated. Truthseeker answered quite cogently several times by pointing out that the basic condition of general ill health and immune system decline would favor the development of various infections, including HIV.

    John and more recently Gene Semon have contributed useful technical comments, which touch on a specific third factor which is characteristic of HIV/AIDS patients and their risk groups: the condition of oxidative stress. This was first pointed out by the leaders of the Perth Group (the Australian scientists who dissent from the HIV=AIDS paradigm) and now accepted by mainstream scientists (including Luc Montagnier, discoverer of HIV, after he read ONE of the Perth papers). Due to the use of oxidizing drugs (such as nitrites) and deficiency of dietary antioxidants and their metabolic products, HIV/AIDS patients show higher levels of oxidative stress, as now is widely recognized.

    Numerous studies have shown that oxidative stress will preferentially diminish CD4 T cells and will also increase viral load of various viruses, including HIV. Antioxidants, such as N-acetylcysteine, selenium and vitamin E, have been shown to produce both increases in the CD4 count and reductions in HIV viral load.

    Another “third factor” is the widespread use of corticosteroid drugs in AIDS risk groups, as well as the endogenous corticosteroid, cortisol, in malnourished subjects. As Dr. Mohammed Al-Bayati has shown in his review of the literature (click HERE), corticosteroids can produce marked reductions in CD4 T-cell counts (as much as -600 cells in 10 days!). Corticosteroids also increase HIV viral load. Let’s hear what Anthony Fauci, director of NIAID, and his colleagues wrote about this:

    “…addition to the cell cultures of…glucocorticoid (GC) hormones, which are known to exert profound immunosuppressive effects, increased both the frequency of positive viral isolation from infected individuals and the levels of HIV replication…” (in New Concepts of AIDS Pathogenesis, L. Montagnier, Ed., Marcel Dekker, Inc, 1993, p. 77).

    (See also: P. Markham et al. Hydrocortisone and some other hormones enhance the expression of HTLV-III. Int J Cancer 37:67-72, 1986.)

  110. Chris Noble Says:

    People can read the Herzenberg paper here

    http://www.pnas.org/cgi/content/full/94/5/1967

    It should be obvious that there is a large spread in CD4 T-cell GSB within both HIV- healthy controls and HIV+ subjects with a large overlap between the two.

    In figure 2 thge authors draw an optimal cut-off at 1.05 on the GSB axis. A large number of healthy HIV- controls have GSB values below this figure and a large number of HIV+ with CD4 counts of less than 200 have GSB counts above it. Although there is a significant difference between the average GSB level in the subgroups an individual GSB value is not that good a predictor of CD4 cell loss.

    In fact the authors make it clear that GSB is lost progressively in HIV disease. It is a result of the HIV infection and not vice versa.

    Oxidative stress is a part of the pathogenesis of many viruses including influenza. It is caused by the virus. So far I haven’t heard any “rethinkers” trying to blame influenza on oxidative stress.

    None of this is in any way a validation of the Perth Group’s thoroughly unscientific ideas no matter how much you try to enlist Montagnier as a supporter.

  111. Truthseeker Says:

    None of this is in any way a validation of the Perth Group’s thoroughly unscientific ideas no matter how much you try to enlist Montagnier as a supporter.

    Chris, the consistent impression you give is that you are incapable of evaluating any scientific idea, only of subscribing to one or another. How would you justify this statement, that the ideas of the Perth Group are “thoroughly unscientific”? It is a gratuitous, shallow insult with no discernible meaning other than that you, Chris Noble, wish to put down their efforts, which have been published in scientific journals of repute, and which have emerged as early and prescient in more than one respect, as indicated by Montagnier.

    This kind of self indulgent dismissal of others’ work needs to be justified by chapter and verse, and specific critique, if it is not to be removed by the NAR software automatically. Especially when it comes from someone whose comments are not nearly as expert scientifically as those he criticizes, which can only irritate other posters.

    Oxidative stress is a part of the pathogenesis of many viruses including influenza. It is caused by the virus. So far I haven’t heard any “rethinkers” trying to blame influenza on oxidative stress.

    This is similarly silly as an attempt at an impolite dismissal. Are you suggesting that oxidative stress cannot be caused by something other than a virus, such as drugs and nutrient deficiencies, to which the immune system is especially vulnerable??

  112. Chris Noble Says:

    This is similarly silly as an attempt at an impolite dismissal. Are you suggesting that oxidative stress cannot be caused by something other than a virus, such as drugs and nutrient deficiencies, to which the immune system is especially vulnerable??

    Oxidative stress is indeed caused by other things than viruses.

    The point is that the Perth Group in a thoroughly unscientific manner attempt to portray the paper by Herzenberg et al as supporting their theory that oxidising agents and not HIV causes AIDS.

    This is simply dishonest. Herzenberg et al are extremely clear – their work demonstrates that HIV causes oxidative stress.

    The Perth Group do no experimental work of their own. Their entire project involves fishing through “orthodox” papers and selectively citing bits that they naively think support their hypothesis. They even try to enlist Montagnier as a supporter of their theories.

    This is exactly the same as the activities of other pseudoscientific groups such as anti-vaccinationists and creation “scientists”.

  113. German Guest Says:

    Truthseeker, could you please delete all messages by Chris Noble that contain the words “creationists” oder “creation scientists”. I really don’t see how this waffle could contribute to our discussion about the causes of AIDS.

  114. john Says:

    Chris,
    The words which you put in the mouth of Herzenberg are a theoretical petition. Nobody demonstrated that hiv causes the oxidative stress. Stalled is simply supposed.
    Otherwise how to explain the multiple interventions of Luc Montagnier and of the Institut Pasteur, which indicate explicitly that we do not know how hiv could provoke it?
    All that you say is only bad science and a nightmare for our world.

  115. nohivmeds Says:

    It seems perfectly logical to think that there are many factors which cause oxidative stress, including viral, bacterial, and fungal infections, drugs used to treat those infections, recreational drugs, severe depression, nutritional deficiencies, etc., etc. HIV does NOT uniquely cause oxidative stress, and therefore, the fact that it does (among so many other variables) cannot be used to argue that HIV causes AIDS. It’s really as simple as that.

  116. nohivmeds Says:

    It does, however, seem that “living in and of itself” causes oxidative stress — like Joe Jackson sang, “everything causes cancer.” Oxidative stress arguments, therefore, are really kind of a wash. What part of living doesn’t cause oxidative stress? Oxidative stress is a normal physiological response. If Perth wants to argue that those with whatever HIV is seem to suffer enormous amounts of oxidative stress — much more than say, those on cancer chemotherapies, they would really have to illustrate that, and I don’t believe they have.

  117. nohivmeds Says:

    In other words, the Perth group’s critique of “what” HIV is, is much more compelling to me than their use of oxidative stress to explain AIDS. And on one point, Chris Noble is entirely correct — Perth are not performing experiments, they are intelligently reviewing and integrating disparate literatures.

  118. pat Says:

    I would like to second German Guests request. The eternal infiltration of comparisons to different “thoughts” such as “creationism”, “anti-vaccinationists” and “other pseudoscientific groups” is totally inappropriate as it is intended as an insult.

    Chris, you are aware of the “Hitler Zombie” back on Orac’s bleuh!-og and rightfully attack it whenever it rears its ugly head. So please don’t let yourself slip here. It is one thing to disagree and another to be disagreeable. Thank you!

  119. pat Says:

    “They even try to enlist Montagnier as a supporter of their theories. ”

    Didn’t he say that HIV alone cannot cause AIDS? But then again he signed the Durban declaration if my memory serves me right. Dead foliage, twisting whichever way the wind blows. Sounds like someone has his balls in a vice I would say.

  120. German Guest Says:

    There was a documentary “AIDS – Die grossen Zweifel” in german/austrian TV some years ago in which was pointed out that HIV-dissidents like Duesberg are condemned to prove not only their “HIV is not sufficent to cause AIDS” hypothesis but at the same time have to deliver some kind of alternative explanation for the cause of AIDS. Otherwise they will not be taken seriously.

    I think the scientific community is not fair in this regard. As long as there is some evidence for an alternative cause of AIDS, there should be an extended discussion about possible factors or co-factors. But unfortunately – as Duesberg complains – such research is forbidden in our scientific community.

    Jon Cohen and others accordingly refuse to accept the findings of the new “viral load of crap” study in JAMA because they further on want to stop the scientific debate about co-factors and alternative explanations for AIDS.

    To my surprise, there are at least some scientists that try to find the real causes of the disease without bias. And they are not afraid to point out that therefore HAART cannot be considered as a preferable therapy for large numbers of AIDS-patients:

    Friday, October 06, 2006,
    Study results raise concern: “Immunologically discordant response to HIV therapy associated with increased risk of disease progression”

    Lutfy MR et al. Increased clinical events in HIV-infected patients who achieve full virologic suppression but fail to attain a CD4 count equal or above 200 cells/mm3 after 1 year of cART. Forty-Sixth Interscience Conference on Antimicrobial Agents and Chemotherapy, San Francisco, abstract H-1403, 2006.

  121. Arthur Gittleman Says:

    I noted Robert Houston has corticosteriods as being bad for treating HIV. He has it backwards. HIV causes overactivation which increase HIV replication and drugs like prednisolone reduce this. Jean-Marie Andrieu has several studies using prednisolone on HIV. Patent No. US5846961 MULTI-FACTED METHOD TO REPRESS REPRODUCTION OF LATENT VIRUSES IN HUMANS AND ANIMALS BY Van Dyke, Knox shows the use on seven FIV cats and one HIV human. Alfred J. Plechner book “Pets at Risk” basis treatment on corticosteriods drug. German doctor recently used prednisolone 5mg daily for many years on his patients. I have used prednisolone at times on my own FIV cats. Prednisolone at low dose is used as a anti-inflammation drug but at high dose creates immunosuppression. As for Dr Fauci; his lab tried using Prednisolone 40mg on HIV study around 1998 and stopped it because the drug produces serious side effects at high dose and not because it is bad for HIV. He should have used low dose. As soon as the Germans can get together more money, it is likely that the use of prednisolone will be one of the standards used to prevent the pregression of AIDS before using HAART.
    I should mention on doctor used dexamethasone and procaine 30mg injection as patient that could no longer use HAART as an alternative for two years in study published.

  122. nohivmeds Says:

    Montagnier is clearly supportive of co-factors, and Gallo seems at least somewhat supportive of the idea in this, their final letter to Harper’s, regarding the Farber article:

    19 May 2006

    Mr. Roger Hodge

    Editor

    Harper’s

    New York, New York

    Dear Editor,

    Misleading statements have been made about the history of HIV/AIDS research in the recent article “Out of Control: AIDS and the Corruption of Medical Science”, (Harper’s Magazine, March, 2006) as well as in some of the replies (Harper’s Letters, May, 2006). The position of us both is that HIV is the essential and sufficient agent that causes AIDS. One of us (Luc Montagnier) has emphasized that there may be (and indeed there are) other factors that can favour HIV transmission (such as co-infection with other sexually transmitted disease organisms) and also promote faster progression toward the clinical stages of AIDS in untreated HIV infected people. Indeed, both of us have contributed to the identification of such factors but this does not put into question that HIV alone is the cause of AIDS. We hope to dispel another point of confusion. It is said that some AIDS patients are HIV negative (an argument made by those who deny the role of HIV in AIDS). This is not the case. First, false negative results are extremely rare nowadays when trained personnel carry out modern diagnostic assays in properly equipped laboratories. Second, there are other causes of severe immune deficiency, such as extreme radiation exposure and rare genetic diseases, just like a severe sore throat can be caused not only by streptococcus, pneumonia not only by pneumococcus, and lung cancer not only by smoking. However, the appearance of a new immune deficiency, AIDS, on an unprecedented, pandemic scale was caused by the spread of HIV within the human population.

    Finally, we would like to emphasize that the major aspects of the history of the discovery of HIV, of the early evidence leading to the conclusion of its causative role in AIDS, and the development of the HIV blood test, have been jointly published by us. We do not have any significant difference in viewpoints on this history. (See Gallo RC and Montagnier, L. The Discovery of HIV as the Cause of AIDS. NEJM, 349:2283-2285, 2003; Montagnier, L. A History of HIV Discovery. Science, 298:1727-28, 2002; Gallo. RC. The Early Years of HIV/AIDS. Science, 298:1728-30, 2002; and, Gallo RC and Montagnier L. Prospects for the Future. Science, 298:167-1834.).

    Sincerely,

    Robert C. Gallo, MD

    Director

    Institute of Human Virology,

    Professor of Medicine and

    Professor of Microbiology and Immunology

    University of Maryland Baltimore

    Baltimore, Maryland

    Luc Montagnier

    President

    World Foundation AIDS Research

    and Prevention

    Paris, France

    Thus, the situation is more severe than german guest implies. The establishment seems to be slowly embracing multifactorial views on AIDS causation — this should imply that the debate is over, but it’s not. That’s because it has become about personalities and politics, and not about science at all.

  123. German Guest Says:

    @ nohivmeds: thank you very much for this important quote!

    One of us (Luc Montagnier) has emphasized that there may be (and indeed there are) other factors that can favour HIV transmission (such as co-infection with other sexually transmitted disease organisms)…

    The content of such statements is zero, nothing, hot air. I would have said exactly the same if I were Montagnier and I had to maintain my reputation after the publication of Celia Farbers article in Harper’s Magazine.

    There’re indeed other factors than “co-infection with other sexually transmitted diseases” such as illicit drugs such as meth and cocaine.

    Gallo and Montagnier would never accept that. But there is evidence! Only two examples. There’re many more:

    1)
    methamphetamine (meth) may act as cofactor in human immunodeficiency virus (HIV)-1 pathogenesis
    Madhavan P. N. Nair et al, Journal of NeuroImmune Pharmacology, September 2006

    2)
    …use of illicit drugs presents a potential risk of decreased resistance to infections in humans. The studies […] suggest that illicit drugs act, at least, as cofactors that can increase the severity of infection by microbial agents by altering host resistance. Because epidemiological data suggest that HIV-positive drug abusers progress to symptomatic AIDS more rapidly additional longitudinal studies addressing the enhancement of disease in immunocompromised individuals are warranted. Guy A. Cabral, Journal of NeuroImmune Pharmacology, September 2006

    But there is another very important level, on which scientific evidence gets thoroughly analysed. You know where???: JUST FOLLOW THE MONEY!!!

    Guess what happened a few days after the publication of the “viral load of crap” paper in JAMA:

    Gilead’s Big Shift
    Peter Kang and Matthew Herper 03/10/06, 6:00 AM ET

    Gilead Sciences announced Monday it will acquire Myogen for $2.5 billion in cash, a whopping 50% premium.

    For Myogen (nasdaq: MYOG – news – people ) investors, who had already seen the stock appreciate to five times its value since two years ago, it is a sweet deal; Myogen shares are only a buck less than the $52.50 purchase price. But Gilead (nasdaq: GILD – news – people ) shares slumped 6.5% Monday on what some viewed as a pricey deal that doesn’t fit into Gilead’s core franchise–drugs to target HIV and other deadly viruses.

    Analysts who cover Gilead were divided on the deal. Bret Holley, an analyst at CIBC World Markets, wrote in a note to investors that the purchase could put to rest some questions about the company’s long-term growth prospects.

    But Geoffrey Porges, an analyst at Sanford C. Bernstein, took an opposing view in an interview. “I don’t like my favorite antiviral company, that’s been focused and disciplined, going off and doing a large, flashy and diversifying deal at a massive premium to what the market thinks the technology is worth,” he says. “How are they going to pull this off? What do they see that the rest of us don’t see?”

    http://www.forbes.com

  124. nohivmeds Says:

    @ german guest — you have identified the central problem. Montaigner, Gallo, any and all of them can admit to co-factors — hell, they can even admit to recreational drug use if they want — none of it will matter one bit. Because the situation is no longer governed by the rules of good science, but instead, by politics, personality, and as you so well describe — by the market. It truly is AIDS, Inc. The science has been sucked right out of it.

  125. Truthseeker Says:

    The point is that the Perth Group in a thoroughly unscientific manner attempt to portray the paper by Herzenberg et al as supporting their theory that oxidising agents and not HIV causes AIDS.

    You were asked, Chris, not to use this phrase “unscientific” as an empty smear, and similarly, one can ask you not to use “creationist” in a like manner. These contentless expressions of your inability and/or unwillingness or both to see the point of others’ work are unwelcome here as causing irritation to other posters and distraction that detracts from the argument, especially since they are characteristically used to bolster statements which are especially questionable, as in this case.

    That oxidising agents in the form of major abuse of drugs and serious lack of key nutrients are causes of the major immune dysfunction that marks “AIDS” has by definition more to recommend it than the claim that HIV causes same, since that hypothesis has so far produced absolutely no evidence at all in the literature that cannot be better explained by the reverse of the paradigm, and over the years a constantly expanding pile of papers falsifying it, the JAMA and the Lancet HAART studies being the latest to break the link between HIV and immune system changes.

    But of course the world is full of influential paradigm promoters and their followers who automatically deny the falsification, and reverse the implication of the results so determinedly that the increasingly Alice Through the Looking Glass hypothesis becomes unfalsifiable, which in Popperian terms in itself proves it unscientific.

    The Perth Group do no experimental work of their own. Their entire project involves fishing through “orthodox” papers and selectively citing bits that they naively think support their hypothesis. They even try to enlist Montagnier as a supporter of their theories.

    More unthinking and misplaced disparagement without meaning in this discussion. There is no reason why experimental work has to be a qualification for reinterpretation of evidence which has been presented in support of an interpretation that doesn’t hold water. Almost the entire critique of HIV∫AIDS lacks new experimental work partly because it is impossible to get funding for any. But this critique doesn’t need any novel experimental support – it doesn’t have to provide an alternative hypothesis to demolish the paradigm as senseless, and the alternative hypothesis has all the evidence it needs in the paradigm literature already published.

    The critique of the paradigm eviscerates the hypothesis on the basis of the paradigm’s own literature, which by itself is self condemning to an extent that for years papers have been characteristically schizophrenic, starting off with a rote bow to the prevailing consensus and then announcing a puzzling fundamental contradiction to it.

    If you insist on your automatic refitting of all such antagonistic data into your fundamentally unexamined belief system by twisting yourself, your mind and the data into a pretzel, feel free, but don’t call others unscientific who actually apply their critical faculties to the material in an openminded assessment of its meaning, rather than with your preconception that HIV must be the cause, which in the final analysis appears to be entirely emotionally driven.

  126. mark Says:

    another VL article

    Another nail in the coffin?

  127. Dave Says:

    Mark,

    Great find!

    I love this quote:

    However some patients who commence antiretroviral therapy experience what is called an “immunologically discordant” response to their HIV therapy. This means that although their viral load is suppressed to undetectable levels, their CD4 cell count fails to increase to above 200 cells/mm3.

    Hmm. And all these years I thought if you killed all those rascally viruses with all these toxic drugs, you’d get big increases in white blood counts!!

  128. Gene Semon Says:

    But let’s watch as Chris Noble takes them out and spits them back at us with his usual display of math prowess.

    As Zen Master Rummy would say to his student Chris, there are known unknowns that must be turned into unknown knowns.

    More from the Herzenbergs: “The activation of nuclear factor kB (NF-kB) has been implicated in the regulation of transcription of a variety of genes and has been shown to be essential for the expression of genes controlled by the long terminal repeat of human immunodeficiency virus (HIV LTR). We show here that intracellular thiol levels play a key role in regulating this process.”

    Gee, I wonder if the Perth Group has anything to say about thiol levels and cellular regulation? But that would be pseudoscience. Of course.

    Continuing: “That is, stimulation with tumor necrosis factor and/or phorbol 12-myristate 13-acetate activates NF-kB and markedly decreases intracellular thiols; N-acetyl-L-cysteine, an efficient thiol source, prevents this thiol decrease and blocks the activation of NF-kB; and the lack of activated NF-kB prevents the activation of the HIV LTR and the transcription of genes under its control.” Could these be the same pol RNAs measured by the branched DNA assay in the paper which is the subject of this thread?

    Now, contrary to science in the Bizarro World, (the unknown unknowns), the fact that retroviral LTRs are cellular promoter regions and subject to the control of cellular transcription factors, here made clear by the Herzenbergs, should be sufficient for all nonbots to see what is effect and what is cause.

    “These findings reveal a previously unrecognized genetic regulatory mechanism in which cytokine-induced shifts in intracellular thiol levels are crucial in the control of NF-kB activity and thereby influence the spectrum of genes expressed by cytokine-stimulated cells.” And this, naturally, has nothing to do with methods of stimulating cells in culture to produce retroviruses.

    FJT Staal, M Roederer, LA Herzenberg and LA Herzenberg; Intracellular Thiols Regulate Activation of Nuclear Factor kB and Transcription of Human Immunodeficiency Virus, PNAS, (1990) Vol 87, 9943-9947

    As always, I’m looking forward to the next mathematical nit he’s going to pick, since I appreciate the lessons in how to scam with statistics.

  129. noreen martin Says:

    Dave, I thought too if the virus was killed or “non-detectable that one would see improvements in the blood counts. I have posted my blood counts with full, blown AIDS, on the HAART and when I stopped the meds. If anyone is interested, they can be viewed at noreenshealthdiner.com.(under bio) I will be posting the reports periodically.

  130. Chris Noble Says:

    More unthinking and misplaced disparagement without meaning in this discussion. There is no reason why experimental work has to be a qualification for reinterpretation of evidence which has been presented in support of an interpretation that doesn’t hold water.

    My criticisms of the Perth Group is that they start with their preconceived ideas and sift through the literature and pull out quotes here and there that they think support their hypothesis. They ignore the majority of papers that provide evidence that contradicts their hypothesis. Often they ignore parts of the paper that they cite when they contradict their hypothesis.

    The exact same behaviour was seen here when you cite the JAMA paper as evidence that HIV has nothing to do with the depletion of CD4 cells when in fact the evidence in it says the opposite. It is hypocritical to take one part of a paper and ignore the rest. It is unscientific.

    The papers written by the Perth Group may be compelling for a lay-audience but are completely unconvincing for anyone that is aware of the totality of research in the field.

    There is an inverse relationship between a persons knowledge of the field and the likelihood of finding the Perth Group’s ideas convincing. I suspect that even Duesberg regards the Perthies as pseudoscientists although he is reticent to say that publicly.

  131. Truthseeker Says:

    There is an inverse relationship between a persons knowledge of the field and the likelihood of finding the Perth Group’s ideas convincing. I suspect that even Duesberg regards the Perthies as pseudoscientists although he is reticent to say that publicly.

    Whether one finds the Perth group’s conclusions convincing or not, your dismissal of their efforts with repeated generalizations of this nature is meaningless given your lack of demonstrated authority ie given your complete lack of known scientific credentials (according to your own postings on another site you are not even a statistician, which is clear enough from your recent comments), your inability to entertain any alternative scientific viewpoint, and your abysmal lack of understanding of what is said to you as exhibited in Comments on this site (Exhibit A currently your lack of understanding of the JAMA paper, in which you still contradict the conclusion of the authors despite several explanations: “Presenting HIV RNA level predicts the rate of CD4 cell decline only minimally in untreated persons. Other factors, as yet undefined, likely drive CD4 cell losses in HIV infection. These findings have implications for treatment decisions.”).

    Therefore you are requested not to express your general opinion of the quality of science perpetrated by other authors without specifics, and preferably even with specifics. That means (we repeat this because you are apparently having difficulty in understanding the requirements of this site even though repeated now four times) you do not express your general opinion on the quality of science of anybody else in the world without demonstrating that you understand the fundamental process of scientific discussion yourself.

    This involves demonstrating something better in scientific argument than the equivalent of examining the dung of an elephant for evidence that its trunk and large ears are an illusion, mistakenly pointed out by other onlookers.

  132. Chris Noble Says:

    Exhibit A currently your lack of understanding of the JAMA paper, in which you still contradict the conclusion of the authors despite several explanations

    You are being dishonest here. I have never contradicted the authors of the paper only your misinterpretation of the paper.

    The authors write: Our findings confirm previous observations that the magnitude of HIV viremia, as defined by broad categories of presenting HIV RNA level, is associated with the rate of CD4 cell loss and extend this observation to patient populations comprising both men and women.

    If you really think that the authors support you interpretation then write to them and see. One of the authors has already made a comment about “rethinkers” misinterpretting the study!

    In fact this could save time. Whenever you come across a study that you think supports your ideas write to the authors and ask them whether your interpretation is correct.

    I really fail to see what you hope to achieve by misrepresenting papers like this. You are not going to convince the authors. You are not going to convince the vast majority of scientists.

  133. Truthseeker Says:

    another VL article

    Another nail in the coffin?

    Looks promising, Mark, thanks. Worth quoting the top paragraph from that aidsmap.con report:

    HIV-positive individuals whose anti-HIV therapy succeeds in suppressing viral load to undetectable levels, but who nevertheless fail to experience an increase in their CD4 cell count above 200 cells/mm3, remain at a high risk of experiencing progression to AIDS and death in the first year of HIV treatment, according to a study presented to the Forty-Sixth Interscience Conference on Antimicrobial Agents and Chemotherapy in San Francisco last week. The investigators, from the University of British Columbia, say that this finding is “concerning”.

    By the way, we have known of this JAMA study problem of baseline HIV load having little to do with progression to AIDS and death since at least 2002, when the Lancet published Egger and May’s paper “Prognosis of HIV-1 infected patients starting highly active antiretroviral therapy: a colloaborative analysis of prospective studies” saying that data on 12,574 adult patients starting HAART with at least three drugs found that “baseline HIV-1 viral load was associated with a higher probability of progression only if 100,000 copies/ml or above” (summary) and in the text “our study showed that at the time of starting HAART the CD4 cell count was a more important prognostic factor than viral load” .. and “in our study, viral load was associated with worse prognosis only if equal to or above 100,000 copies/ml”.

    That paper by the way said “we stress that in addition to HAART the introduction of prophylactic treatments against opoprtunistic infections will have contributed to the observed improvement in prognosis.”

    So a) “viral load is crap” and b) “HAART needs help”.

  134. Truthseeker Says:

    In fact this could save time. Whenever you come across a study that you think supports your ideas write to the authors and ask them whether your interpretation is correct.

    But our “dishonest” “interpretation” was simply to accept the summary conclusion as quoted. Your inability to distinguish the meaning and significance of the two quotations – yours and ours from the same paper – and to think you have to choose between the two is your own very odd problem, not that of the authors or the “vast majority of scientists”, though it is always possible the vast majority of scientists do not perceive any more clearly than you do.

    Certainly, we would never use the judgement and understanding of “the vast majority of scientists” as a criterion of the truth of any paradigm, unlike yourself, since by definition progress in science through the overthrow of a ruling paradigm is only achieved against the judgement and understanding of the “vast majority of scientists”. Perhaps you should spare a moment to contemplate how you could shift to a higher plane of mental operation if you wish to continue discussing whether this paradigm is correct or flawed. The level of “the vast majority of scientists” is not good enough.

    In the case of the JAMA study and its meaning if you cannot distinguish between the general and the particular in this paper’s statements describing what they found you have to study it more carefully, since there have been sufficient Comments here to help you do so and yet you ignore them.

    What is there about “interindividual variability” that you do not understand?

    What is there about this statement that immediately follows the one you quote (which was: “The authors write: Our findings confirm previous observations that the magnitude of HIV viremia, as defined by broad categories of presenting HIV RNA level, is associated with the rate of CD4 cell loss and extend this observation to patient populations comprising both men and women.”) that you do not understand?

    Despite this association, however, only a small proportion of the interindividual variability in the rate of CD4 decline can be explained by plasma RNA level, even after accounting for the effect of measurement level.”

    The fact that you quarrel with the authors of the study in saying that the two statements are contradictory is a matter for you to take up with the authors, not us.

    What is our concern is that you waste the time and attention of people following this blog trying to gain some enlightenment and fresh information by repeatedly serving up stale fish that you do not even cook. It is your responsibility to study and understand the parts of a study which you feel are contradictory, and resolve the contradiction yourself, writing to the authors if you need to, and if you raise the point here, to listen to and deal with the answers respectfully, just as we respond to you respectfully if you do so.

    Accusations of dishonesty and being unscientific do not have any content whatsoever if you do not understand the material being discussed. The only appropriate attitude is one of humility until you do master it, which is an essential task anyway because otherwise the discussion stalls. But to both quarrel with the statements of the study authors and also to accuse us of misrepresenting it by using direct quotation is absurd.

    In fact it is so foolish that it is lovable in mildly charming way, so there may be some value in that, we grant you. In fact, thank you for your willingness to be foolish, Chris, it does alleviate the seriousness of the topic, which can always do with a little humor. We had you down as totally earnest, but perhaps you are not.

    Perhaps you don’t care about being right that much, if you are willing so easily to be wrong. Perhaps you are just having fun by trying to trip up HIV∫AIDS critics wherever you can find them, and don’t really care what they say, or you say, as long as it puts a spanner in their gears.

    What fun you must be having, Chris, and so cheaply, too. So much attention for so little investment. And you don’t even have to know what you are talking about!

  135. German Guest Says:

    Thank you Chris Noble,

    for educating us about the way HIV/AIDS-believers are trying to bring forward their weak arguments!

    A few days after the JAMA-study was published I took part in a few stormy debates about HIV, viral loads and antiretroviral treatment with HAART. This was a lot of fun and very revealing. Most people almost all-automatically told me that despite the results of the JAMA-study HAART MUST BE EFFECTIVE!. Why? Simply because it is said to be the only HIV-treatment available and so many people are on HAART. There is a very, very strong believe in the power and altruistic engagement of pharmaceutical companies.

    Of course I was prepared, and after a lot of aha-experiences on both sides we all agreed that HAART is – at least – not advisable for HIV+ people who don’t suffer from serious, life-threatening illnesses for the simple reason that HAART itself is damaging and life-threatening.

    For me it is not important to convince people that HIV is not the cause of AIDS. I want to convince HIV+ people that HAART is not a cure for AIDS. I want to encourage them to question their doctors orders and to look for more information about lifesaving therapies and wholesome attitudes. Let’s get it straight: HAART is nothing more than a multi-billion-dollar-business!

    And I am very much convinced that you, Chris Noble, are part of this business.

  136. Robert Houston Says:

    Whether or not Mr. Noble is a part of the “multi-billion-dollar-business” of HIV drugs and treatment, he certainly has acted as a predictable spokesman of AIDS orthodoxy, spinning any study to make it appear to support their dogma and maligning any critics of the faith.

    While he tries to present the Sept. 27th JAMA study as a ringing endorsement of the HIV=AIDS connection, the reality is that the study called it into question. The authors concluded: “The results of our study challenge the concept that CD4 cell depletion in chronic HIV infection is mostly attributable to the direct effects of HIV replication.” In fact, they found that HIV levels had little predictive value. “These findings represent a major departure from the notion that plasma HIV RNA level is a reliable predictor of rate of CD4 cell loss in HIV infection and challenge the concept that the magnitude of viral replication…is the main determinant of the speed of CD4 loss at the individual level.”

    In contrast, when confronted with the Herzenberg 1997 study of the benefit of glutathione and N-acetylcysteine (NAC) against oxidative stress in HIV patients, Mr. Noble wrote, “Although there is a significant difference between the average GSB level in the subgroups, an individual GSB value [glutathione measurement] is not that good a predictor of CD4 cell loss.” This is the exact opposite argument from the one he used regarding the JAMA study. In actuality, his analysis missed the main point of the Herzenberg study of the antioxidant NAC, which was that “subjects who took NAC were roughly twice as likely to survive for 2 years as the subjects who did not take NAC…(P=0.019)” (L. Herzenberg et al. Proc. NAS 94:1967-72, 1997).

    Anthony Fauci and colleagues also studied glutathione and NAC and found that these antioxidants suppressed HIV expression in vitro. They concluded that “therapy with thiols may be of value in the treatment of HIV infection” (Suppression of HIV expression… by glutathione… and N-acetylcysteine. T. Kalebic et al. Proc. NAS 88:986-90, 1991). They pointed out that “GSH [glutathione]…protects cells from oxidative damage and…also plays a critical role in immunoregulation.”

    This is similar to what Eleni Papadopulos, professor of medical physics and leader of the Perth Group, had proposed years before, in suggesting the use of antioxidants such as thiols to counter the oxidative stress characteristic of AIDS. Prof. Peter Duesberg, by the way, thought enough of the scientific expertise of her and the Perth Group to invite two papers from them, which were featured as the first chapters in a scholarly book he edited (AIDS: Virus- or Drug Induced?, Ed.: P. Duesberg, Kluwer, 1996).

    Having read an early paper of hers, HIV’s discoverer Luc Montagnier later wrote on the issue, but failed to give her credit (see E. Papadopulos, Med. Hypoth. 67:666-68, 2006). In fact, Montagnier became the chief editor of a book on the subject (L. Montagnier et al., Eds., Oxidative Stress in Cancer, AIDS and Neurodegenerative Diseases. Marcel Dekker Inc. 1998). In his autobiography, he devoted a section to “Oxidative Stress” and wrote:

    “According to the hard-core virologist, the virus kills the T4 cells it infects and the whole disease springs from that. This is a naive and simplistic conception that betrays a certain intellectual ridgidity or quite simply an ignorance of everything that happens to fall outside one’s narrow area of specialization…

    “What happens in patients suffering from AIDS? One notes a significant shortage of antioxidants and a rise in oxidation products: the level of glutathione in the lymphocytes decreases, peroxidized lipids appear in the blood, proteins are oxidized… The phenomenon is massive and occurs at an early stage… all opportunistic agents can likewise contribute to oxidative stress, and from the very onset of the infection, so can mycoplasmas… We know that the products of this stress trigger cellular apoptosis… This has led us at the Pasteur Institute to begin tests with antioxidants and to study their effects on apoptosis and on the evolution of the disease. The first results, obtained with N-acetylcysteine, a precursor of glutathione, have been encouraging.” –Luc Montagnier (Virus, Norton, 2000, pp. 183-185.)

  137. Chris Noble Says:

    The fact that you quarrel with the authors of the study in saying that the two statements are contradictory is a matter for you to take up with the authors, not us.

    Where have I said that they are contradictory?

    You keep on trying to say that I have contradicted the authors.

    I’ll quote Michael Lederman again.

    “The idea that our findings published today in JAMA can be taken to support the concept that HIV is not the cause of AIDS is ludicrous. The role of HIV as the cause of AIDS has been proven over and over again. Clearly the people who are misrepresenting our work are not only incapable of clear thinking, they are also apparently unable to read.”

    I have contradicted nothing in the paper. I have argued against your particular spin of the paper in a vain attempt to use it to argue that HIV does not cause AIDS.

    Your arrogant assertion that you can interpret the paper better than the authors is astonishing.

  138. Truthseeker Says:

    But Chris, we just answered at some length your claim that you could interpret the paper better than the authors. Are you not aware of that? Did you not understand what we wrote? Was it too complex for you to understand?

    If you don’t understand why the author wrote to Bennett the sentence you quote, which is not from the paper, and cannot remember that we told you that such flag waving was de rigeur nowadays when you publish awkward results, we can only ask you not to reply until you have mastered the material.

    You have to understand the politics as well as the science to address this topic productively. If you cannot master either, then you must ask for assistance here or among your colleagues, who no doubt will be glad to assist.

    The initial posts of this blog explain the basic concepts.

  139. Chris Noble Says:

    But Chris, we just answered at some length your claim that you could interpret the paper better than the authors. Are you not aware of that? Did you not understand what we wrote? Was it too complex for you to understand?

    You are still being dishonest. There is nothing that I have said that has contradicted anything in the paper or written by the authors. You on the other hand continue to misrepresent the paper.

    If you don’t understand why the author wrote to Bennett the sentence you quote, which is not from the paper, and cannot remember that we told you that such flag waving was de rigeur nowadays when you publish awkward results, we can only ask you not to reply until you have mastered the material.

    Is this your pathetic excuse for continuing to misrepresent the paper?

    You have to understand the politics as well as the science to address this topic productively. If you cannot master either, then you must ask for assistance here or among your colleagues, who no doubt will be glad to assist.

    The initial posts of this blog explain the basic concepts.

    I have to ask again. Who are you hoping to convince?

    Your initial post was written before you had read the paper. I read the paper before I responded. It was obvious that your interpretation was false. It is obvious to the vast majority of scientists.

  140. pat Says:

    It appears to be true that Chris is not contradicting what is in the paper. It is simply fortunate for him that the paper contradicts itself.

    “The idea that our findings published today in JAMA can be taken to support the concept that HIV is not the cause of AIDS is ludicrous. The role of HIV as the cause of AIDS has been proven over and over again. Clearly the people who are misrepresenting our work are not only incapable of clear thinking, they are also apparently unable to read.”

    This little gem is political talk. They merely slip this in to cover their asses from what they have actually found.

  141. Dan Says:

    Pat,

    good observation.

    Truthseeker aptly named HIV=AIDS the “look away” paradigm a while back.

    This is yet another example of the “look away” paradigm.

    (Believe this honor belongs to someone else, though the thought was shared.- Ed.)

  142. Dan Says:

    This little gem is political talk. They merely slip this in to cover their asses from what they have actually found.

    Smells (stinks) like Padian.

    Here’s how she spins it: “HIV is unquestionably transmitted through heterosexual intercourse. Indeed, heterosexual intercourse is now responsible for 70-80% of all HIV transmissions worldwide”

    Now, somebody refresh my memory. How many seroconversions were observed in her study of discordant couples?

  143. pat Says:

    ehm…ehm…it’s on the tip of my index fingers…ehm…

  144. Truthseeker Says:

    What is this, Chris, a comic turn? All your points have been spiked, and yet you continue to repeat them, as if nothing was true but saying made it so.

    Let’s give you the correct version of this study point by point:

    1) The AIDS meme cannot be a premise of the discussion

    Yes, our initial post was written on the basis on reports of the study before reading the study, and hey presto!, the study was even worse for the reputation of paradigm supporters than reported. You quote a standard disclaimer of one of the authors that the results are not embarrassing for the paradigm. But Chris, that is what we are discussing. If you cannot entertain the idea that this is possible, if your responses can only consist of turning a blind eye to the study itself, and the statements of the authors in print in the study, we can only admire your imitation of Nelson at Trafalgar, but we cannot productively discuss the point, since your premise consists of denying what is under discussion, so discussion cannot proceed.

    It is rather as if you continued resolutely informing us that the moon is made of green cheese, you know that for a fact, Dr Gallo and Dr Fauci say so, despite NASA sending up a rocket manned with astronauts who bring us back a sample of its soil.

    2) The study says HIV does not govern CD4 loss

    What precisely is there about the following words you do not understand?

    “The results of our study challenge the concept that CD4 cell depletion in chronic HIV infection is mostly attributable to the direct effects of HIV replication. Future efforts to delineate the relative contribution of other mechanisms will be crucial to the understanding of HIV immunopathogenesis and to the ability to attenuate it.

    That is the conclusion of the study, in the paper, ending the paper, in toto. Do you not understand it? In lay translation, it says the following: “When CD4 cells go down in an “AIDS” patient, this is hardly due to HIV, it is mainly (90%) due to other factors. HIV does not have a significant direct impact on the level of CD4 cells. Other factors are the ones responsible, and we must find out what those other factors are.”

    Perhaps you need even that translated. OK, it means this. Evidently HIV does not govern immune system collapse, other factors do, 9 to 1. Any reassuring group correlation between CD4 and HIV perceived by Chris Noble or other HIV∫ AIDS diehards is if causal actually demonstrating the reverse of the paradigm assumption that HIV leads to CD4 loss. It is CD4 loss that leads to more HIV replication, not vice versa.

    3) Study explodes the main pillar of the paradigm

    Understand, Chris? No? OK, what is there about the following words you do not understand?

    “These findings represent a major departure from the notion that plasma HIV RNA level is a reliable predictor of rate of CD4 cell loss in HIV infection and challenge the concept that the magnitude of viral replication (at least as reflected by plasma levels) is the main determinant of the speed of CD4 loss at the individual level.”

    “Major departure”. “Challenge the concept”. Translation: HIV doesn’t govern CD4 loss. Main paradigm pillar knocked out.

    4) So don’t attack with HAART

    Oh, but the group experience is different, right? You cling to that idea, like a drowning man clnging to an inflated raft when the liner has upended and vanished to the bottom. You find it in the study, after all, as the above quote continues:

    The clinical implications are that in the majority of case, an individual patient’s plasma HIV RNA level at the time of presentation for clinical care cannot predict, to a significant extent, the rate of CD4 decline that he or she will experience over the subsequent years and is therefore of limited clinical value in shaping the decision to initiate antiretroviral therapy.

    In other words, DON”T start HAART just because HIV RNA level is high in the blood plasma, folks, it means nothing as far as your future rate of CD4 loss is concerned. That is dependent on OTHER factors. And what are those other factors, Chris? What other factors could be affecting the immune system in a pill popping, night clubbing, multi-multi-partner, food skipping gay urban male? Or poor urban black, given HAART? What?? you may say. HAART itself cause CD4 decline? No! That cannot be! It is HIV that causes CD4 decline. Well, Chris, read this study and contemplate which comes first, a rise in HIV viremia or a CD4 decline. It tells us that CD4 decline comes first.

    5) Group correlation IF causal could go either way

    Anyhow, to continue the quote:

    This is despite the fact that a group of individuals with an approximately similar level of plasma viremia will, on average, tend to lose CD4 cells at a faster rate than another group with a lower level of viremia, a previously reported finding that stands uncontested by our results”

    Hooray, you cry, that’s what I was talking about, group by group, the higher the viremia, the higher the CD4 loss. But Chris, you dogged little terrier you, stop growling and clamping your needle sharp teeth on our trouser cuff long enough to get this: it says nothing about the direction of the causation, if any. It is a correlation, and the direction of causation, if any, or linkage, is not determined. It could be a rise in HIV viremia leads to CD4 loss. Or it could be CD4 loss results in greater HIV viremia.

    6) Other factors are causing CD4 loss

    And this is precisely what the study and the study authors throw light on. The lack of predictability from HIV to CD4, a mere 10 per cent correlation, if that, in an individual, indicates OTHER FACTORS govern CD4 loss, and THEREFORE the direction of cause if any is that CD4 loss precedes a rise in HIV viremia, NOT vice versa.

    7) Blinded by the AIDS meme, it’s a “puzzle”

    Maybe you should study the accompanying editorial by Keith Henry et al in the same issue of JAMA, page 1523, if you are still having difficulty in accepting what is going on.

    Its title is “Explaining, Predicting, and Treating HIV-Associated CD4 Cell Loss: After 25 Years Still a Puzzle”. Now what does this title mean, Chris? It means this, in lay translation:

    If the HIV∫AIDS paradigm (HIV causes AIDS because HIV causes CD4 cell loss) is still the inviolate assumption, then after 25 years we still have no idea how to explain this paper’s result. “Clinicians treating patients with HIV encounter some patients with low plasma viral levels who experience rapid progression.” But how can this be? “What mechanism is responsible for their profound and quick CD4 loss?” Since we know that HIV is responsible for AIDS, and nothing else is, it cannot be OTHER FACTORS. Don’t even mention the possibility, or Dr Fauci will come and beat you with a very large stick. So it is still all a “puzzle”.

    So “What factor(s) explain the other 90%? Twenty five years into the HIV epidemic, a complete understanding of what drives the decay of CD4 cells–the essential event of HIV disease–is lacking.” Of course it is lacking, if you persist in the premise that AIDS and CD4 loss is “HIV disease”. There is no explanation on God’s earth for it because there is no evidence for it! The evidence is for OTHER FACTORS causing the immune deficit, with HIV playing no part. But as long as you persist in the idee fixe that HIV is responsible for the damage, you will find your understanding is “incomplete” – because it will be non existent.

    8) Avoiding Dr Fauci’s very big stick

    And why are these members of the high powered “vast majority of scientists” that you are so in awe of, Chris, so fond of this “HIV is the only cause”, Gallo-eian premise? Could it be that it is a sine qua non of funding? Could it be the money trail, Chris? Could that be why this petty point, this obvious elephant in the room, staring them in the face and treading on their toes, is invisible to them, and yet plain to any outside observer, even your untutored faithful blogger, who does not share the same blinkers, as you apparently do, Chris, for reasons unknown to the assembled company here, but possibly due to funding considerations, since you do not deny it, and that seems to be the only possibility as to why such a clever, mentally active, logically impeccable, doggedly truth seeking, determinedly problem solving person such as your distinguished self cannot see even the outline of the answer to the “puzzle” Keith Henry et al wrestle with, which all outside independent obervers can see in two minutes, since they are free of this assumption, this AIDS meme, that all is a consequence of HIV, and no OTHER FACTORS are causal, a concept that causes the faithful to shriek with horror at the prospect of Dr Fauci’s wrath.

    9) JAMA comment says it is NOT the virus

    What is it about the following sentence from the Keith Henry comment that you do not understand?

    The findings by Rodriguez et al provide support to those who favor non virological mechanisms as the predominant cause of CD4 loss; however, these data should be interpreted with caution, and the issue of a single viral load as a prognostic marker should be separated from the role of viral replication in HIV pathogenesis.”

    Do you not understand these words? Here is a lay translation: OTHER FACTORS and not HIV are the cause of most of the CD4 loss. But Dr Fauci, don’t blame us, we still believe in HIV killing CD4 cells and causing AIDS. We believe, Dr Fauci, we believe!

    The meaning of this is clear to anyone who frees themselves from the AIDS meme, the assumption that all is somehow caused by HIV. And the meaning is that HIV is not a significant factor in causing CD4 decline.

    10) Blather: symptom of the AIDS meme

    Such a person can observe the following paragraph of Keith Henry’s with amused recognition of the meme at work:

    “Direct and indirect effects of HIV infection, not fully measured by plasma HIV RNA levels, reverberate through a host’s unique genetic and immunologic environment. HIV persists in the issues throughout the body and likely sets off chain reactions of acute and chrnic immune disturbances. Some of the mechanisms involved in this process most likely have been identified, but it is uncertain whether these factors are independent of one another, driven directly by the virus (or indirectly by the state of chronic immune activation ssociated with HIV infection), or a combination of both. In many cases it is difficult to elucidate what is cause and what is effect in these observations.”

    If you cannot recognise this as blather, then there is very little hope for you, Chris. A lay translation is this: We imagine without proof that HIV is causing all kinds of disturbances which we cannot understand or elucidate using our assumption that HIV is the cause, and we are not even going to mention the possibility of abandoning that completely unproductive and unproven assumption, in case Dr Fauci thinks we are undermining one of the greatest pork barrels in the history of biology.

    11) Bottom line: paradigm bombed at base

    The fact that the study demonstrates that HIV does not govern CD4 loss in an individual is the equivalent of a truck bomb at the base of the tower that is HIV∫AIDS, and it is time to get out of the building, Chris. You could be very valuable as an objective observer.

  145. Dave Says:

    Bravo, Truthseeker!

    You have dispatched Chris Noble with the intellectual equivalent of the Rodney King beating:)

    Can we lay odds that his next feeble post will be something along the lines of …

    But, Truthseeker, HIV still causes AIDS!

    Question to Chris:

    When Dr. Henry writes:

    The findings by Rodriguez et al provide support to those who favor non virological mechanisms as the predominant cause of CD4 loss

    What “non-virological mechanisms” do you think he’s talking about?

  146. pat Says:

    <b>those who favor non virological mechanisms</b> sounds so much better than…ehm, re-thinker…denialist

  147. Truthseeker Says:

    You have dispatched Chris Noble with the intellectual equivalent of the Rodney King beating:)

    Thank you Dave, but we prefer a more kindly comparison, especially since the thought police are all on the other side. We are trying to enlighten Chris and win him over to climbing to a higher perch, instead of parroting from inside the HIV∫AIDS cage. Then he might come fly with us, high over the forest, so that he can see the forest and not the trees, and squawk with joy at the dazzling new insight opened up for him, and become the guru he was always meant to be, to whom all those who seek knowledge attend – the world’s greatest authority on the paradigm, and its senior attendant when it is finally parked like the Concorde on a barge in the East River.

    His new perch can be on its nose.

  148. kevin Says:

    Chris Noble:

    Now what is your explanation for figure 1 in the recent JAMA article that is supposedly the subject of this thread?

    For those who are tired of hearing Mr. Noble exalt the importance and overwhelming power of Figure 1 in the JAMA study, I’m providing a link to the most thorough treatment of this little chunk of data that I’ve yet read. I hope the original author doesn’t mind and that it isn’t bad manners to link to another blog? Perhaps, even Mr. Noble will be compelled to read it and comment here since the other site does not permit comments on this article. Anyway, here’s the link:

    http://tinyurl.com/egk67

    I’m not sure that it is even necessary to answer “the Figure 1” mystery after Truthseeker’s thorough undressing of Mr. Noble’s denialism (used in the literal sense here, not the HIV=AIDS pejorative). However, I found the above link quite informative and exceedingly helpful in deciphering the double-speak that has accompanied much of the public discussion about the implications of this study.

    Kevin

  149. Chris Noble Says:

    Let’s give you the correct version of this study point by point:

    Thank you for the lesson in how not to read a paper. You get a mark of 0 out of 11.

    The spin you put on this paper just reveals your preconceived notions.

    I eagerly await the publication of your letter in JAMA.

    I would also recommend that Darin Brown also submits his spin piece to JAMA.

    Honestly the arrogance of people like you that think they can interpret papers better than the authors is astounding.

  150. Truthseeker Says:

    The spin you put on this paper just reveals your preconceived notions.

    Chris, sadly, we are forced to recognize your status as permanently intellectually and emotionally challenged by the task of reading and understanding this blog and this Comment thread, as advertised and confirmed by this striking four part demonstration of your inability to read and understand even a very long comment devoted to your better grasp of what is going on, where every concession is made to your difficulties, and every point is explained at exhaustive length not only in lay terms but even a second time in baby talk.

    You are now reduced it seems to repeating back to us like a parrot the basic corrections we tried to make to your responses. You simply repeat back to us in your post above, and in the post above that, the four key points in what we told you ie that a) you are arguing against the authors of the study and b) you have not read the paper properly, c) if you disagree with the authors you should write to the authors or JAMA and d) you cannot see around your preconceived notion that the paradigm is inviolable.

    This is in fact the second time that you have done nothing but simply reverse our strictures and in an adult version of the schoolyard response of “Same to you!” parroted back to us what we said about you.

    So we are forced to conclude that it is not possible to get you to do anything but a) parrot the paradigm and b) parrot our points back to us. Regretfully, therefore, we are forced to treat you as a parrot, give you a peanut and hand you off to your cage perch, where you can better amuse Dr Fauci and Dr Gallo by repeating what they say without comprehension of its inadequacy.

    This is very disappointing since we have always found that your contributions here have been extremely stimulating, forcing us to explain things very very simply, which of course is of immense use to us in double checking what we think and say and also a benefit to readers who don’t have time to get into the spurious complications of this essentially silly and blatantly obvious scientific issue, or work out what the heck you mean when you misinterpret the papers you claim to believe in.

    We hope that you will continue to make such stimulating contributions in the future where your misapprehensions can be corrected for the benefit of all, but beg you to avoid the parroting mode, since it doesn’t have any content that can profitably be discussed by others here.

  151. Chris Noble Says:

    You simply repeat back to us in your post above, and in the post above that, the four key points in what we told you ie that a) you are arguing against the authors of the study and b) you have not read the paper properly, c) if you disagree with the authors you should write to the authors or JAMA and d) you cannot see around your preconceived notion that the paradigm is inviolable.

    a) I am not arguing against the authors of the study. You are.

    b) Michael Lederman has made it clear “Clearly the people who are misrepresenting our work are not only incapable of clear thinking, they are also apparently unable to read.”

    c) You are the the one that is disagreeing with the authors.

    d) You are dreaming.

    I wish you well with your delusions of adequacy.

  152. Truthseeker Says:

    Chris, we have begged you not to be a parrot, and here you are doing it again, so all we can do is offer you a peanut and stroke the top of your head against the feathers, which is what parrots like, which we know on account of having our own grey parrot here, who sends his greetings in the form of a whistle.

  153. nohivmeds Says:

    I find the discussion with Noble somewhat ridiculous regarding interpretations of the JAMA paper. As I was trained, it was made quite clear to me that 5 of the best scientists in a particular area could sit down, look at a paper, and come out with 5 equally plausible interpretations. Mr. Noble – there is no “correct” way to interpret a paper — and the authors’ interpretations are not necessarily the “correct” interpretation either. The authors of any paper clearly always have biases in interpretation, and dislike it when others interpret their work in varying ways, but THAT IS HOW THINGS WORK IN SCIENCE. You can dislike someone’s interpretation, but I don’t see anything here in TS’s interpretation that you can invalidate, and the authors’ opinions make little difference in this.

    Might I suggest this: Mr. Noble only agrees with interpretations that are consistent with the AIDS meme. He allows for no possible interpretations that differ from that conception, yet this ignores one basic issue in science, which is that findings may be interpreted in any number of ways, all logical and coherent. That is simply a fact, Mr. Noble. And it has made for fascinating scientific debate for decades now, in every existing area of science. I’m afraid that it is you who really demonstrates a lack of understanding of the role of interpretation in science.

  154. YossariansGhostbuster Says:

    Well, while ya’all are whistling past the graveyard, Chris is as close to a clearer explanation of the JAMA article as anyone else. TS is still throwing hamburger helper to the puppies whilst he yet drives another rubber nail for some buddies paradigm.

    Yossarian has looked at this carefully and hath discover’d the following truth not quite ready for the history channel:

    It is not clear how much of the pathology of AIDS is directly due to the virus and how much is caused by the immune system itself, but the JAMA article people are actually going in the appropriate direction for which they ought not be driven into
    NAR’s bull dozer.

  155. Gene Semon Says:

    It’s interesting how the “comeback kid” consistently ignores any branching points in the discussion that may lead to a wider world, such as my previously-posted response to the concluding sentence of the JAMA RNA/CD4 paper.

    In the Bizarro World, it is simply understood that “future efforts” are necessary to consider “other mechanisms”, “non-virological”, since our esteemed JAMA authors’ seem totally oblivious to the efforts of others who have already proposed them in numerous peer-reviewed publications. Adding to Robert Houston’s excellent post is Roberto Giraldo’s thorough review, “NUTRITIONAL THERAPY FOR THE TREATMENT AND PREVENTION OF AIDS: SCIENTIFIC BASES”. (http://www.robertogiraldo.com/ => eng/papers/NutritionalTherapy_SADC_2003.html)

    Excerpt: “There is today a growing number of scientific publications indicating that oxidizing stress is an absolute requisite for both testing positive on the tests for HIV (201-207) and for developing the clinical manifestations of AIDS (208-230).

    “Free radical reactions of special significance to immunological phenomena are, for example, the many oxidizing agents that can abstract a hydrogen atom from thiol groups to form thiol radicals (231-233). Thiol groups are important for enzyme activities, receptor functions, disulphite links in immunoglobulins, and T cell activation and proliferation. The super oxide anion radical can react with nitric oxide, resulting in loss of endothelium-derived relaxing factor activity, which is important in the inflammation/disinflammation process. Methionine oxidation can cause protein damage with subsequent changes in immunogenicity. Proteolysis can be increased by free radical damage. The per oxidation of lipids by reactive free radicals produce many biological modulators such as, for example, the 4-hydroxy-alkelans, which produces strong chemotactic activity for phagocytes, alters the adenyl cyclasa system, increases capillary permeability, and alters lymphocyte activation. Lipid hydroperoxides, also from per oxidation of lipids, alter lymphocyte activation. Conditions favoring lipid per oxidation may result in chemo taxis of leukocytes, protein modification, immune complex injury, and cell death (231-233).

    “Free radicals are produced throughout the regular immune system network. Despite the beneficial effects of the inflammation responses, they can also aggravate existing tissue damage by releasing free radicals. When uncontrolled, initiated by an abnormal stimulus, or occurring for prolonged periods of time, inflammation may become a disease process (231-233). It is critical for optimal immune responses that there be a balance between free radical generation and antioxidant protection. During phagocytosis by polymorphonuclear leukocytes, for example, super oxide anion radicals are released. These oxygen free radicals can oxidize thiol groups to thiol radicals, and can stimulate lipid per oxidation with the formation of H2O2, which is highly significant in the mechanisms of cell injury. Oxygen free radicals produced during phagocytosis of immune complexes are associated with injury to immune complexes (231-233).

    “It has often been proposed that free radicals and specifically oxidizing species play important roles in the pathogenesis of AIDS (189-200,234-236).

    “The above are the scientific fundamentals for the use of antioxidants such as vitamin A and carotenoids, vitamin C, vitamin E, selenium, n-acetyl cisteine, l-gluthamin, zinc, cooper, manganese, alphalipoic acid, coenzyme Q10, and flavonoids or vitamin P, as supplementation for the prevention and treatment of AIDS (48,188-236).”

    Note the 49 references and number 230, “Staal FJT et al. Antioxidants inhibit stimulation of HIV transcription. AIDS Res Hum Retroviruses 1993; 9: 299-306”. Again, this makes clear to a literate person – meaning one doesn’t have to ask the authors that it confirms the Perth Group – what is cause and what is effect.

    The wider world also includes, “Mitochondria and Cancer, by Professor Serge Juragunas, Townsend Letter – August/September 2006”, which has relevance to AIDS and is “based on the notion that mitochondria can indeed regulate genomic activity”. Additionally, “mitochondria have been shown to play a crucial role in the regulation of apoptosis and the maintenance of cellular redox, which regulates growth … at the cell surface of specific signal transduction pathways, which in turn induce crucial transcription factors to regulate genes essential for cell growth.” The article continues the above discussion on the pathogenic effects of oxidative stress as they relate to the mitochondria and represents a neat synthesis with some of the new findings in regulatory genomics.

    Unfortunately, too many biomolecular scientists – especially those who directly perceived the ultimate truth of the JAMA RNA/CD4 article, as Chris has explained to us – are clueless when it comes to the above.

  156. YossariansGhostbuster Says:

    Wouldn’t you know it, Capt’n Crunch Gene Semon shows up with yet another oxidation theory on cluelessness.

  157. Robert Houston Says:

    Gene Semon has provided a valuable resource in highlighting the magnificent 2003 review by Roberto Giraldo, M.D., on “Nutritional Therapy for the Prevention and Treatment of AIDS”, which contains 315 references. Another very useful paper of his is “‘Co-factors’ cause AIDS”, which surveys the many oxidative and immunological stressor agents that can lead to immune deficiency.

    Snide remarks by “YosariansGhostbuster” (AKA McKiernan) are offbase and ill-informed (e.g., “oxidation theory on cluelessness”). As I documented in my previous Comment, even HIV discoverer Luc Montagnier agrees that oxidative stress is a major factor in AIDS and can be moderated by antioxidants, a view similar to the Oxidative Stress Theory of AIDS which was first proposed in the 1980s by biophysicist Eleni Papadopulos-Eleopulos, leader of the Perth group of dissenting scientists centered in Australia. In a new scientific publication, she discusses the similarity of Montagnier’s views and her original theory (click HERE).

    In his memoirs, Montagnier objected to the common practice of virologists to attribute all phenomena in AIDS to HIV. He termed this “a naive and simplistic conception” and pointed out that “all opportunistic agents can likewise contribute to oxidative stress…so can mycoplasmas” (Virus, W.W. Norton Co., 2000, pp. 183 and 185). The Perth Group has long pointed out that recreational drugs, dietary deficiencies and other lifestyle factors characteristic of AIDS risk groups can produce oxidative stress. Furthermore, the very low levels of actual HIV virus in AIDS patients, which NIAID director Fauci has estimated affect on average only 1 in 1000 T-cells, means that any effect of HIV “envelope proteins” (such as TAT) on oxidative stress would be miniscule compared to the onslaught of strong oxidizing agents such as nitrite drugs and corticosteroids common in HIV/AIDS risk groups.

    Glutathione, a peptide containing the amino acid cysteine, is a major antioxidant in the body and helps protect T-cells from oxidative damage. Its levels are known to fall in AIDS. A Stanford University study found that oral supplements of the glutathione precursor N-acetylcysteine (which is now available in every health food store) resulted in a doubling of the survival time of AIDS patients (L. Herzenberg et al. Glutathione deficiency is associated with impared survival in HIV disease. Proc. NAS 94:1967-72, 1997). Other antioxidants, such as selenium, are relevant to the glutathione defense (see the Giraldo review).

    Contrary to a typically misleading claim of Chris Noble on this thread, Herzenberg et al. did not attribute the drop in glutathione (GSH) in AIDS solely to HIV. On the contrary, they wrote that “multiple mechanisms may contribute to systemic GSH deficiency in HIV disease, including excessive production of inflammatory cytokines and excessive use of GSH-depleting drugs.” They advised that “the unnecessary or excessive use of acetaminophen [e.g. Excedrin], alcohol, or other drugs known to deplete GSH should be avoided by HIV-infected individuals” (see abstract).

    It’s also pertinent that while Herzenberg et al. in 1997 measured “total GSH”, additional research in Norway found that a variable more predictive of AIDS progression and CD4 decline was “”increased levels of oxidized glutathione and a decreased ratio of reduced [non-oxidized] to total glutathione” (F. Muller et al. Thiols to treat AIDS. In: Nutrition and AIDS, Ed.: R. Watson, 2nd Edition, CRC Press, 2001, p. 79).

  158. Chris Noble Says:

    I find the discussion with Noble somewhat ridiculous regarding interpretations of the JAMA paper. As I was trained, it was made quite clear to me that 5 of the best scientists in a particular area could sit down, look at a paper, and come out with 5 equally plausible interpretations. Mr. Noble – there is no “correct” way to interpret a paper — and the authors’ interpretations are not necessarily the “correct” interpretation either.

    There is indeed often room for a large amount of interpretation in any paper. This does not mean that any interpretation is as valid as any other. Postmodernism has not managed to take over science – so far. Some interpretations are better than others and some are just plain wrong where they specifically contradict results in the paper.

    TS’s interpretation was formed before he read the paper. He did not base his interpretation on the totality of the results in the paper. In particular his interpretation contradicts the results in figure 1. The idea that the paper falsifies the idea that HIV causes AIDS is frankly ridiculous. This interpretation is inconsistent with the results.

    Any valid interpreation needs to provide some explanation for the data in figure 1. Ignoring it is not good enough. Claiming that it is not statistically significant is also not good enough – it clearly is. When pushed some of you came up with alternative explanations for the relationship between HIV viral load in subgroups and the rate of depletion of CD4 cells. None of these alternatives were plausible.

    While the authors of an article do not have the final say on the interpretation of their results their opinion has much more credibility than that of an innumerate journalist who does not have access to the information that the researchers have. If you are going to stand up and claim that your interpretation is more valid than that of the authors you would be advised to actually learn a bit more mathematics and science. Resorting to political arguments is not valid. It might convince an audience prone to conspiracy theories but it won’t convince the majority of scientists.

    The authors have made a further clarification here.

    http://www.aidstruth.org/rodriguez-lederman.php

    TS has repeatedly claimed that I have contradicted the authors of the paper. This is clearly not so. This is simply a silly rhetorical trick and is frankly bizarre.

    TS’s rhetoric might work well in the small enclosed world of HIV “rethinkers” where everybody slaps each other on the back for their brilliant insights and laugh at the thousands of scientists that are stupid enough to believe that HIV causes AIDS but it just won’t wash in the real world

  159. Chris Noble Says:

    Contrary to a typically misleading claim of Chris Noble on this thread, Herzenberg et al. did not attribute the drop in glutathione (GSH) in AIDS solely to HIV.

    Is there a school that you have all attended where you can learn the art of misreading? I have never made that claim.

    In fact it is clear that a significant number of healthy HIV- controls also had low GSH levels.

    GSH levels on their own are not a good predictor of who is going develop AIDS. In HIV+ people there was an observed relation on average between GSH levels in CD4 cells and progression to AIDS.

    The “interpretation” that the Herzenberg paper is evidence against the role of HIV in AIDS is also ludicrous.

  160. Truthseeker Says:

    There is indeed often room for a large amount of interpretation in any paper. This does not mean that any interpretation is as valid as any other. Postmodernism has not managed to take over science – so far. Some interpretations are better than others and some are just plain wrong where they specifically contradict results in the paper.

    At last, a correct statement from Chris. This is a cause for celebration. We agree with every word, and shudder to think what “I’m OK, you’re OK” science would lead to, if unleashed.

    As to the rest of your comments, however, we can only say, Chris, you are repeating yourself yet again, without any greater effect than before. Same old inability to understand Fig 1 as anything but a contradiction of what the authors say. The problem, however, is that what you are repeating is wrong. It is, as another distinguished poster characterized it, “typically misleading”. Your denialist (of reason and evidence) mode has lost its regulator, and now you apply it even to a study you believe supports your religion.

    Chris, you cannot at one and the same time support and deny the quoted conclusions of the authors, claim that a figure in the study supports your denial, and say that our agreement with their conclusion is ludicrous. You are chasing your own tail, and will soon spin ever faster into a blur that will deliver you into another universe altogether, an alternate reality where HIV causes AIDS. But then, that is the one you believe in so steafastly, it appears, so you will be happy there, we imagine.

    Anyway we welcome this self-exposure of yours, this parade of repeated “same to you” schoolboy denial of what is obvious to everyone else. It illuminates your determinedly denialist (of reason and evidence against HIV) mode, your refusal to take in new information, or to understand repeated explanations of material which baffles you. Your piteous repeated cries of “please explain Fig 1” are very moving. We wish we could help. But apparently words are not enough.

    So these are our last on the subject and we hope, yours too. There comes a point where repetition is redundant to the point of migraine.

  161. nohivmeds Says:

    One does not need postmodern thought to recognize the fact that data can be validly interpreted in a number of ways. Postmodernism had absolutely nothing to do with the argument I made — science did.

    The authors of an article are, contrary to what CN would like to think, often the worst authorities on their own work — that is an inescapable fact. Researchers set out to do a study with particular assumptions (many unknown to them) guiding their choices of method and interpretation. If authors were the best representatives of their work, there would be no need for peer review, or science journalism, for that matter. But human subjectivity does inevitably interfere with all interpretations — especially those of the original researchers, as they have more invested in the correctness of their interpretations than do other readers. Simple, really. Basic psychology, nothing more.

    CN raises one interesting point that was raised during the EJ Scovill catastrophe — TS, would you, as Christine Maggiore insisted she was, be ready to reject your current frame and accept HIV as causal in AIDS if you were presented with the proper evidence? If not, then CN is correct in asserting that you are likely as biased as he is. All good scientists leave a great amount of room for the possibility that they are utterly wrong. All good commentators on science should do the same.

  162. Dave Says:

    This is a great question by nohivmeds:

    would you, as Christine Maggiore insisted she was, be ready to reject your current frame and accept HIV as causal in AIDS if you were presented with the proper evidence?

    It shouldn’t be limited to TS, though, it should be propounded to all folks who are skeptical of the virus theory.

    The converse question should also be propounded to viral proponents as well:

    would you be ready to reject your current frame and reject HIV as causal in AIDS if you were presented with the proper evidence?

    And, of course, then follow up questions, ie, What would be “proper evidence?” etc, etc would ensue, and then, holy smokes, there’d be intelligent back and forth on this critical issue.

  163. Truthseeker Says:

    If authors were the best representatives of their work, there would be no need for peer review, or science journalism, for that matter. But human subjectivity does inevitably interfere with all interpretations — especially those of the original researchers, as they have more invested in the correctness of their interpretations than do other readers. Simple, really. Basic psychology, nothing more.

    Well said. Interpretation is typically subjective to some extent, humans beings being what they are, emotional enough to keep psychologists in business for another few decades at least. You are quite right to point this out, especially since it is a major factor in keeping the HIV∫AIDS fantasy rolling. This doesn’t mean that all interpretations must be allowed equal credibility, however, in a sort of scientific democracy, where everyone has one equal vote. Interpretations must reviewed critically, as you also state. But are authors “often the worst interpreters of their work”? Interesting to hear a psychologist say that, since you must be talking mostly about psychology, we assume.

    Anyhow, in this case, the authors of the JAMA paper seem to be clear headed about the significance of their data, and about the awkward politics of it. It is only CN that seems muddled, and to think that their disclaimer is purely scientific. Our own interpretation, of course, is purely objective. We are the single exception among all commentators in that respect. We are surprised you haven’t noticed this.

    CN raises one interesting point that was raised during the EJ Scovill catastrophe — TS, would you, as Christine Maggiore insisted she was, be ready to reject your current frame and accept HIV as causal in AIDS if you were presented with the proper evidence? If not, then CN is correct in asserting that you are likely as biased as he is. All good scientists leave a great amount of room for the possibility that they are utterly wrong. All good commentators on science should do the same.

    If that means we are rated a “good commentator”, we hurry to get out the green border for your comment. But to answer your query, the answer is tautological, isn’t it? “Accept HIV as causal in AIDS if you were presented with the proper evidence”? By definition, we would have to, no? What you may mean is, do we argue from a bias, as CN does, and always pick out what we conceive to be in line with our overall conclusion – in his case, that HIV causes immune deficiency which causes AIDS, in our case, there is no evidence for that yet, and every evidence that AIDS is caused by familiar factors such as drugs, malnourishment, and disease itself? Do we pick out these data, and ignore the rest?

    The answer is no, in fact, we are not particularly invested in toppling the paradigm, if anyone would care to present a single good theoretical pillar of support for it. In many ways, it would be convenient if someone did that, and we could all pick up our marbles and find some less obvious issue to discuss. Convenient in the practical sense of use of time, energy and money, and avoidance of repetition. The fact that grown men sit around nitpicking the dung of an elephant and discussing whether it exists or not when it is standing right behind them is the real interest in this topic, as you, a psychologist, obviously see. So it has to be acknowledged there would be that loss – of the greatest example of human foolishness extant in the present age.

    There would be other disappointments associated with that ending, too, of course. It is always a boost to one’s vanity to see more clearly than other people, and recognize the elephant they cannot see behind them. But that sort of self satisfaction wears off fairly rapidly, we find, especially since a know-it-all is liable to get punched on the nose even if he is right. It would be much better if everyone saw the elephant, lives could be saved, and money and time devoted to something more constructive.

    Besides which, as CN shows, the same secure feeling of being right and knowing better is shared by everyone in this discussion, no matter which side people are on.

    By the way, connoisseurs of foolishness should hurry over to trrll’s comment, just up over at the “In Europe, fish oil after heart attacks – but not here” post (Click HERE). In his view he has completely demolished Peter Duesberg’s set of HIV∫AIDS’ failed predictions, and single handedly rescued the paradigm from its most damaging challenge. Foolish, foolish Duesberg! Clever, clever trrll!

  164. Robert Houston Says:

    Having been exposed in his attempt to misrepresent a study, Mr. Noble compounds his error by now claiming that he made no such statements. Here’s our recent exchange:

    Houston (10-12-06, 11:56 pm): Contrary to a typically misleading claim of Chris Noble on this thread, Herzenberg et al. did not attribute the drop in glutathione (GSH) in AIDS solely to HIV. .

    Noble (10-13-06, 12:28 am): Is there a school that you have all attended where you can learn the art of misreading? I have never made that claim.

    Now here are Mr. Noble’s actual words in making “that claim”:

    Noble (10-9-06, 2:27 am): People can read the Herzenberg paper here… In fact the authors make it clear that GSB [a measure of glutathione] is lost progressively in HIV disease. It is a result of the HIV infection and not vice versa.

    And this is what the authors of the study actually wrote:

    Herzenberg et al. (Proc NAS 94:1967-72, 1997): Multiple mechanisms may contribute to systemic GSH deficiency in HIV disease, including excessive production of inflammatory cytokines and excessive use of GSH-depleting drugs.

    The authors also stated that “lower levels of GSB (a…measure of GSH in CD4 T cells) predict decreased survival…the probability of surviving 2-3 years increases dramatically as GSB levels approach normal range.” Contrast that with Mr. Noble’s latest misstatement in suggesting that the study indicates that glutathione (GSH) levels are “not a good predictor.”

    The doubling of survival with higher glutathione apparently means nothing to an HIV true believer, but that 4-6% predictive value of HIV viral load is really something to trumpet!

    For a sound analysis by a real mathematician regarding the recent JAMA study on the poor predictive value of HIV measures, see the new article at Barnesworld by Darin Brown, Ph.D. on “Correlation coefficients, viral loads and T-cell dynamics” (click HERE). Dr. Brown points out that “there is no correlation between viral load and CD4 cell loss to speak of. Almost none of the loss of CD4 counts can be explained by viral load levels. The rest of the paper is nothing more than an attempt to obscure this central fact.”

  165. Chris Noble Says:

    The doubling of survival with higher glutathione apparently means nothing to an HIV true believer, but that 4-6% predictive value of HIV viral load is really something to trumpet!

    On average survival rate increased with glutathione levels. At the individual there was a large variation even in the healthy control group with a significant number of healthy individuals having low glutathione levels.

    On average subjects with HIV viral load measurements above 40,000 copies/ml had almost a fourfold higher CD4 cell depletion rate than those with a viral load below 500 copies/ml. Despite all the waffling by Darin Brown the difference is mathematically significant and won’t go away.

    If Darin Brown has a valid criticism of the paper then he should send it to JAMA for publication.

  166. Truthseeker Says:

    On average subjects with HIV viral load measurements above 40,000 copies/ml had almost a fourfold higher CD4 cell depletion rate than those with a viral load below 500 copies/ml. Despite all the waffling by Darin Brown the difference is mathematically significant and won’t go away.

    Chris, we strongly advise you not to try driving in the UK, since you apparently have no concept of direction.

    If Darin Brown has a valid criticism of the paper then he should send it to JAMA for publication.

    Brown is merely pointing out what the paper actually says, not that it is wrong. Are you even aware of the difference? For example, in connection with your favorite peg to hang your hat on:

    At first I was perplexed trying to reconcile Figures 1 and 2. Each gives the median random-effect model estimate of CD4 cell loss/mm^3/year. However, the two data sets are quite different. The data in Figure 1, quoted in the abstract, are 20.2, 39.3, 47.7, 55.9, and 77.7 cells/mm^3/year for the 5 subgroups of increasing HIV RNA level. However, Figure 2 gives the data 37.3, 42,8, 45,8, 48.9, and 52.2 and there is significant overlap between the cell loss rates in different subgroups, which would indicate that the “simple relationship on average between viral load and rate of CD4+ cell depletion” is not supported. The difference between the two data sets is that the data for Figure 2 were computed using the same model for the entire data set, while for Figure 1, each subgroup was studied in isolation and different random-effects models were used for each subgroup.

  167. Chris Noble Says:

    Chris, we strongly advise you not to try driving in the UK, since you apparently have no concept of direction.

    Are you denying that the results showed that people with a high viral load (>40,000 copies/ml) showed a much larger CD4 depletion rate than those with a low viral load (
    This difference is statistically significant.

    Brown is merely pointing out what the paper actually says, not that it is wrong.

    Compare the paper :

    Our findings confirm previous observations that the magnitude of HIV viremia, as defined by broad categories of presenting HIV RNA level, is associated with the rate of CD4 cell loss…

    with Brown’s comment:

    the “simple relationship on average between viral load and rate of CD4+ cell depletion” is not supported

    Despite your crazy hallucinogenic rhetorical contortions it is Brown that is contradicting the paper and it’s authors. Any assertion to the contrary is evidence of a psychological disorder.

  168. nohivmeds Says:

    CN wrote:

    “Despite your crazy hallucinogenic rhetorical contortions it is Brown that is contradicting the paper and it’s authors. Any assertion to the contrary is evidence of a psychological disorder.”

    Now, Dearest CN, I know you’re not a psychologist or psychiatrist, so that was simply a cheap shot at another commentator at the expense of an entire field of study — which only goes to illustrate your desperation and inability to be open to alterntative interpretations. That, in itself, does not constitute evidence of a psychological disorder, but keep making statements like the one above, and you just might get there. And I’d be sure to let you know, of course, if you had provided me enough evidence to saddle you with a diagnosis.

  169. nohivmeds Says:

    And to TS: I agree entirely that not all interpretations are equally valid — if I had made that argument (which I was accused of making), then I would have been making the postmodern argument which deconstructs science to nothing more than a series of interpretations. Again, I am not making that argument.

    As for whether or not the authors are the worst representatives of their own work — this is only more obvious in psychology, but permeates every scientific field, to be sure. Think about cold fusion, for example.

  170. Robert Houston Says:

    Isn’t monomania a psychiatric disorder? Could the whole field of HIV/AIDS be suffering from it? How else to explain a monolithic fixation that is obliged to interpret all phenomena in terms of a single virus and that excludes from consideration any and all other potential influences on the illness, even well-known factors (such as drug abuse, corticosteroid exposure, and nutrient deficiencies) which have been demonstrated to be rampant in the risk groups and fully capable of causing profound immunodeficiency in their own right?

    As a case in point, when confronted by the doubling of patient survival with the enhancement of a natural antioxidant (glutathione), HIV devotee Noble dismissed this as unimportant compared with an association of HIV viral load with a surrogate marker ! He also steadfastly ignored Figure 2 of the new JAMA report, which shows that a 1000-fold increase in viral load is associated with only a 15 cell decrease in CD4 count, i.e., only 3% of the average total count. (Dr. Darin Brown, a mathematician, pointed out in his recent article that valid subgroup comparisons require that the same mathematical model be applied to all, as was the case in Figure 2 but not Figure 1, which involved “separate models to produce estimates [of] CD4 decline for each HIV RNA stratum,” according to the authors.)

    Be this as it may, the authors of the Sept. 27 JAMA report on the (non) “predictive value of plasma HIV…” have opened the locked door a tiny crack. In their stirring reaffirmation of the faith at Aidstruth, Drs. Benigno Rodriquez and Michael Lederman, sing paeans of tribute to the sacred doctrine in terms bordering on religious fanaticism (e.g., “There is absolutely no doubt that HIV is the cause of AIDS”). But heretofore the tacit or even explicit corollary has been to the effect that “there are no other causes or influences worth mentioning,” i.e., “thou shalt worship no other gods.” At the very end, however, the authors append a summary that seems like a plea to let a thousand flowers bloom. They conclude:

    “Levels of HIV in blood explain only a small portion of the variability in the rate at which CD4 T cells are lost. Therefore… Expanded efforts to identify the other elements that drive CD4 cell losses in chronic HIV infection are needed.”

  171. james Says:

    http://www.altheal.org
    taken from above and below
    http://www.aidsmythexposed.com general section thread titled viral-load doesnt predict cd4

    You might want to read this statement by Rodriguez (JAMA: viral load) and Lederman:

    http://www.aidstruth.org/rodriguez-lederman.php

    “There is absolutely no doubt that HIV is the cause of AIDS.”

    “Our results imply that although HIV infection drives the progressive immune deficiency of AIDS (as evidenced by the response to successful treatment with anti-HIV medicines, which decrease the viral load, increase CD4 cell numbers, and prevent or help resolve opportunistic infections, reflecting an improvement in immune function), there must be other intervening elements that cause progressive CD4 cell losses in HIV infection.”

    “The next obvious question is, “What are the other elements in the fuel mixture that are driving the engine?” We think that this will soon be illuminated. Stay tuned.”

    XXXXXXXXXXXXXXXXX

    The elemant is oxidative enviromental level coupled with low antioxidant levels, either through Eleni’s theory, reduction of apoptosis, shifts rebalancing of th1 th2 balances modulated by oxidation and GSH, cell migration , thymus gland atrophy due to oxidation Or a cobination of all of these or possibly others , but the element behing all of these is low antioxidants particulary GSH, selenium and ongoing increased oxidative, lipid peroxidation levels.

    So the answer is the same what ever you care to think .stop oxidative exposures and address the antioxidant defiencies, the cd4 goes up regardless of viral load , diseases are inhibited, patients put on more weight, have fewer infections and less hospitalisations.

    I just wanted to ram this point home and add a little more data and a reference for that selenium study. Please note the “viral-loads” went down in the combo group and the combo plus selenium group at the SAME rate, so the “viral-loads” in both groups where the SAME and the auther states “Our finding that selenium did not have an effect on viral load levels” however the CD4 rise in the selenium plus combo group was approx 2 and half times that of combo alone, thus the rise in CD4 has nothing to do with “viral-load”, thus this plus al the other studies proves that rises in levels are not related to or caused by the “viral-load” levels but rather high levels of oxidation and low levels of antioxidants like GSH and selenium among others.

    The study examined the impact of selenium supplementation in Nigerians with advanced disease who are on HAART. One hundred and seventy one people with HIV on ART were randomized to receive 200micrograms of selenium daily and 170 people with HIV to receive antiretroviral therapy alone. All patients received an antiretroviral regimen of d4T/3TC and nevirapine.

    HIV viral load, CD4 counts, hematological and biochemical indices were measured at the start of the study (baseline) and then every three months. At each visit, adherence and nutritional counseling were given. Patients were followed for 72 weeks.

    Among the 340 subjects recruited with advanced disease, CD4 cell counts were < 50 cells/mm3.

    Although the median time for undetectable viral load was similar in the two groups (p = 0.2), PLWA on HAART + selenium showed the following distinct advantages over those on HAART alone:

    The rate of CD4 cell recovery was significantly higher; median CD4 count increment from baseline to 72 weeks was almost twofold higher in patients on supplementation (+120 cells/mm3 versus +50 cells/mm3).

    The incidence of opportunistic infections were lower resulting in fewer hospital visits.

    Weight gain was significantly higher (p = 0.004).

    Haemoglobin increment from baseline to 64 weeks was 3-fold higher (+30 g/l versus +10g/l).

    Selenium supplementation resulted in a higher CD4 count response and had a significant impact on the quality of life as evident by weight gain, hemoglobin increment, and fewer hospital visits.

    The study suggests that selenium might be a useful complement to HAART in the management of people with HIV with severe immunosuppression, said Dr N Odunukwe, presenting the study.

    She cautioned that selenium should not be considered as an alternative to antiretroviral therapy: “Our finding that selenium did not have an effect on viral load levels does not suggest that it can be given instead of ART,” she emphasised.
    (ADDED BY JAME 🙂 selenium has no impact on “viral-load” but it doubles the cd4 ? Oh really is that dissociated non corralation between cd4 and “viral-load” yet again LOL funny how antioxidants often seem to that )

    This subject was debated in the censored and banned BMJ debate, By eleni, Mr Christopher, others and myself and in the altheal paper by John kirkham.

    In the following threaad you will find papers that show 1.Diseases get better before “cd4” goes up and before “viral-load” go down or “undectable”, you will find papers that show that “cd4” rises strt before “viral-load” drops and that drugs like “hiv” protease inhibitors despite “viral-failure/resistance” keep on inhibiting apoptosis thus preserving or even increasing “CD$4” despite “viral-failure/rebound/resistance”.

    In the KS thread there apers that show they work on non “hiv” type KS.

    They also some how reduce/buffer oxidative stimuli of chemicle, radiological origin.I.E. they are some how sometimes having antioxidant increasing effects.
    xxxxxxxxxxxxxx

    ceramide,apoptosis,antioxidants,”cd4″,Atrophy,combo?

    “Eleven, asymptomatic, HIV-1-infected subjects, who refused any antiretroviral treatment despite experiencing a progressive decline of CD4 counts, were treated with daily infusions of L-carnitine (6 g) for 4 months.” (57) “L-carnitine therapy resulted in an increase of absolute CD4 counts, which was statistically significant on day 90 and 150 (P = .010 and P = .019, respectively). A positive, not significant trend was also observed even in the change in absolute counts of CD8 lymphocytes. L-carnitine therapy also led to a drop in the frequency of apoptotic CD4 and CD8 lymphocytes. This reduction occurred gradually, but changes in actual values between each time point and baseline were strongly significant (P = .001 at the end of the study compared with the baseline). A strong reduction (P = .001) in cell-associated ceramide levels was found at the end of the study. In general, HIV-1 viremia increased slightly. No toxicity related to L-carnitine therapy was observed and dose reductions were not necessary. In HIV-1-infected subjects, long-term infusions of L-carnitine produced substantial increases in the rate and absolute counts of CD4 and, to a lesser degree, of CD8 lymphocytes. This was paralleled by a reduced frequency of apoptotic cells of both subgroups and a decline in the levels of ceramide. No clinically relevant change of HIV-1 viremia was observed.”(57).

    “Lymphocytes from subjects infected with the human immunodeficiency virus type 1 (HIV-1) undergo an inappropriate programmed cell death (apoptosis), a major mechanism for the decline of CD4 and CD8 cells that is crucial to the progression towards the overt acquired immunodeficiency syndrome (AIDS).1-8 Indeed, lymphocyte apoptosis correlates with disease progression and lower CD4 counts: a high degree of apoptosis has been detected in patients with AIDS in comparison with long-term nonprogressors.1-8.”(57).

    “Patients with AIDS have significantly higher lymphocyte-associated ceramide levels than healthy individuals and HIV-1-infected long-term nonprogressors have less elevated lymphocyte-associated ceramide levels than subjects with evolving disease.8,20,21 Remarkably, this is paralleled by a lower frequency of apoptotic CD4 and CD8 cells in long-term nonprogressors than in patients with AIDS.8,21”.(57)

    “All of the subjects reported, with no exception, a sense of improved well-being by the second week of L-carnitine treatment.” (57).

    “The analyzed individuals represent a unique population of infected subjects, all of whom were living in the Community of San Patrignano, being exposed to the same environmental influences and with comparable nutritional regimens. Remarkably, in the majority of individuals, there was a past history of HBV or HCV infection and no opportunistic infection was detected during the trial period.”

    “Taken together, our data suggest that long-term L-carnitine administration may have a substantial impact on the chief immunologic abnormality associated with HIV-1 infection, the loss of CD4 T cells, through downmodulating the generation of ceramide and reducing the rate of apoptotic lymphocyte death, without affecting the HIV-1 viremia levels, thus suggesting that a dissociation exists between changes in viremia and CD4 depletion.” (57)

    Evidence has existed since 1997 and before that the “viral-load” is or can be dissociated from the CD4 depletion, in the study sited above which has been deliberatley ignored by “aids” “science” because it blows a massive indesputable hole in there stupid over simplified religious “hiv” theory. All these 100% patients had declining CD4’s for months before L carnitine/antioxidant infusion, in all 100% of patients they had significant increases in CD4 with either no change no decline in “viral-load” or even increases in “viral-load” with NO SIDE EFFECTS accept all patients had fewer infections, fewer hospital admissions and 100% reported feeling better, “aids” “sciences” and medicines answer to this syudy was either to ignore it or even censore it. In the link to the ceramide thread you will find studies that show that the CD4 increases in people on P.I. based combo start long before the “viral-load” load decreases and that when “drug-failure” /”viral-resistance-rebound-increase” takes place the P.I. based combo’s continue to reduce/inhibit apoptosis-cell death sustaining the cd4 level regardless of the increase in “viral-load”.

    If “aids” science was science and not a greedy ,corrupt, religion , real scientist would of done larger in vivo human research into antioxidants like l carnitine study which would of provided us with very clear cut answers, they didnt because they didnt want to know that the cd4 is dissociated from “viral-load”, there wouldnt of been any risk either because there was NO toxicity reported, no side effects and its cheaper than the toxic expensive “arv’s”.

    So we have tunnle vision and religion running medicine and “aids” “science” afraid of questions, afraid of debate and afraid of been proven how wrong they are.

    Antivir Ther. 1999;4 Suppl 3:7-11.

    Sustained CD4 responses after virological failure of protease inhibitor-containing therapy.

    Deeks SG, Grant RM.

    University of California and San Francisco General Hospital, San Francisco, California, USA. sdeeks@php.ucsf.edu

    This article explores current controversies related to ‘discordant’ responses to antiviral therapy, that is to say, patients with a sustained CD4 cell response despite virological failure. Observational clinical data of patients receiving protease inhibitor-based therapy who had a sustained CD4 cell count even with incomplete viral suppression will be presented, as well as possible mechanisms and clinical implications.

    Publication Types:
    xxxxxxxxxxxxxxxxxx

    The Journal of Immunology, 2003, 170: 6006-6015.
    Copyright © 2003 by The American Association of Immunologists

    Mitochondrial Membrane Hyperpolarization Hijacks Activated T Lymphocytes Toward the Apoptotic-Prone Phenotype: Homeostatic Mechanisms of HIV Protease Inhibitors

    “A decrease of mitochondrial membrane potential has been hypothesized to be a marker of apoptotic cells, including activated T lymphocytes. It was recently demonstrated that HIV protease inhibitors, independently from any viral infection, can hinder lymphocyte apoptosis by influencing mitochondrial homeostasis”

    “They also suggest that HIV protease inhibitors, by interfering with induction of the mitochondrial hyperpolarization state, can result in cell survival even independent of any viral infection”

    ” In contrast, some in vitro and ex vivo studies suggested that PIs, independent from any viral infection, were able to inhibit PBMC loss and to restore impaired T cell proliferative response (16). Accordingly, apoptotic cell death of both HIV-infected and uninfected cells was apparently inhibited. ”

    xxxxxxxxxxxxxxxxxxxx

    Clinical &Experimental Immunology
    Volume 118 Issue 3 Page 412 – December 1999
    doi:10.1046/j.1365-2249.1999.01076.x

    “HAART may increase CD4+ T cell counts despite a persistently detectable HIV load. The impact of HAART on apoptosis, which may play a role in the disease process in HIV-infected patients, has not been extensively studied”

    “We did not observe any correlation between the HIV viraemia and the level of apoptosis of T cell subsets. patients with HAART showed a lower percentage of apoptotic CD4+ T cells only: 16% (range 261%) versus 25% (range 573%) for patients receiving two nucleoside analogues (P = 0.02). T”

    “In conclusion, HAART, without any relation to plasma viraemia, is able to reduce apoptosis of CD4+ T cells. ”

    xxxxxxxxxxxxxxxxxxxxxxxx

    Decreased HIV-associated T cell apoptosis by HIV protease inhibitors.

    Phenix BN, Angel JB, Mandy F, Kravcik S, Parato K, Chambers KA, Gallicano K, Hawley-Foss N, Cassol S, Cameron DW, Badley AD.

    Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ontario, Canada.

    “Emerging evidence suggests that some of the improvements in CD4+ T cell number that occur in response to protease inhibitor (PI) therapy may not be accounted for solely by enhanced viral suppression, implying that PI may directly affect T cell survival”

    “8 days of PI therapy in HIV-infected patients does not significantly alter plasma viremia, yet results in significant inhibition of CD4+ and CD8+ T cell apoptosis. The inhibitory effects of PI on apoptosis have implications concerning the treatment of HIV and its pathogenesis.”

    xxxxxxxxxxxxxxxxxxxx

    Front Biosci. 2004 Jan 1;9:338-41.

    Antiretroviral therapy influences cellular susceptibility to apoptosis in vivo.

    Cooper CL, Phenix B, Mbisa G, Lum JJ, Parato K, Hawley N, Angel JB, Badley AD.

    Division of Infectious Diseases, The Ottawa Hospital-General Campus, Ottawa, ON, Canada. ccooper@ottawahospital.on.ca

    It has been proposed that antiretroviral therapies (ART) possess both antiviral and immunomodulatory activities when used in HIV infected patients.Few studies have addressed whether these putative immunomodulatory effects are also seen in HIV negative patients, for example, when used for post exposure prophylaxis (PEP). We chose to evaluate immunologic function in HIV negative patients who received Nelfinavir and Combivir (AZT and 3TC) as PEP. Lymphocytes from patients taken immediately before, during, and after PEP were analyzed. No changes were seen in absolute or percent CD4 or CD8 T lymphocyte numbers, nor in markers of activation, memory, or co-stimulatory molecules. Surface expression of apoptosis-related ligands and receptors were unaltered, but apoptosis susceptibility was significantly inhibited by PEP (P less than 0.05). These data confirm in vitro that apoptosis susceptibility is altered by ART, including in HIV-negative patients who take PEP.”
    xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx

    http://www.bloodjournal.org/

    Human Immunodeficiency Virus Type 1 Protease Inhibitor Modulates Activation of Peripheral Blood CD4+ T Cells and Decreases Their Susceptibility to Apoptosis In Vitro and In Vivo
    By Elaine M. Sloand, Princy N. Kumar, Sonnie Kim, Aniruddho Chaudhuri, Frank F. Weichold, and Neal S. Young

    .” In this study, we examined the effect of protease inhibitors on Fas-R (CD95), ICE (caspase 1) expression, apoptosis, and cell death in CD4+ T cells of (1) HIV-infected patients who were receiving protease inhibitors, and (2) normal and patient CD4+ T cells cultured with a protease inhibitor in vitro. Fifteen patients with advanced HIV disease on treatment showed dramatically decreased CD4+ T-cell ICE expression, diminished apoptosis, and increased numbers of CD4+ cells within 6 weeks of institution of protease inhibitor therapy, and before down-modulation of Fas-R (CD95) expression was evident. To determine the role of HIV infection, we studied the effect of ritonavir, a protease inhibitor, on normal and patient cells in vitro. Stimulated and unstimulated normal CD4+ T cells, cultured with protease inhibitor, demonstrated markedly decreased apoptosis and ICE expression (P = .01). While Fas-R expression was not significantly altered during short-term culture by such treatment, Fas-Ligand (Fas-L) membrane expression of phytohemagglutinin (PHA)-stimulated blood lymphocytes was decreased by protease inhibitor. In the presence of ritonavir, CD4+ T cells from HIV-infected patients showed similar changes in ICE intracellular levels without alteration of Fas expression. In conclusion, protease inhibitors appear to decrease CD4+ T-cell ICE expression and apoptosis before they affect Fas-R expression in HIV-infected patients. This action was independent of HIV infection, as similar effects were seen in CD4+ T cells from normal controls. ”

    Some of the benefit of protease inhibitors may be related to modification of programmed cell death, which increases CD4+ T-cell number.

    ” However, clinical data suggest that the beneficial consequences of protease inhibitors persist even after viral resistance to the drug has developed,20 and these drugs may thus affect the immune system, independent of their inhibition of retroviral replication. ”

    “In vitro experiments, using CD4+ T cells from normal uninfected controls, showed similar significant declines in ICE expression, apoptosis, and cell death when lymphocytes exposed to Fas agonist or cultured in the absence of IL-2. Protease inhibitors may thus exert effects on apoptosis, independent of their effects on HIV, by affecting directly or indirectly the generation of active ICE protein in the apoptotic pathway. ”

    “One implication of our findings is that inhibitors of ICE or CD4 apoptosis, without antiviral activity, may have potential therapeutic utility in the treatment of HIV infection, even in patients with low viral loads.”

    Antivir Ther. 2005;10 Suppl 2:M29-45.

    HIV protease inhibitors prevent mitochondrial hyperpolarization and redox imbalance and decrease endogenous uncoupler protein-2 expression in gp 120-activated human T lymphocytes.

    Matarrese P, Tinari A, Gambardella L, Mormone E, Narilli P, Pierdominici M, Cauda R, Malorni W.

    Department of Drug Research and Evaluation, Istituto Superiore di Sanita, viale Regina Elena 299-00161 Rome, Italy.

    It has been demonstrated that HIV protease inhibitors (Pls) are able to inhibit apoptosis of both infected and uninfected T cells
    xxxxxxxxxxxxxxxxxxxxxxx

    http://www.bloodjournal.org/

    Blood, 15 March 2001, Vol. 97, No. 6, pp. 1898-1901
    CORRESPONDENCE

    To the editor:
    T-cell apoptosis in HIV-1-infected individuals receiving highly active antiretroviral therapy

    Recently, Lu and Andrieu1 stated that the HIV-1 protease inhibitors (PIs) indinavir and saquinavir used in concentrations at least 30-fold lower than those needed for 90% viral inhibition apparently do not influence sensitivity of peripheral blood T cells from HIV-1-infected individuals toward apoptosis induced either by T-cell receptor/CD3 ligation or by direct triggering of the CD95 receptor in vitro.1 They conclude from their data that the beneficial effect of PI treatment on clinical and immunological parameters in HIV-1-infected patients, which can be encountered even in the absence of relevant virological effects, are not related to changes in T-cell apoptosis.

    In our own study in a cohort of HIV-1-infected children and adolescents, we had observed an increased sensitivity of freshly isolated T cells toward apoptosis,2 which was rapidly down-regulated following initiation of highly active antiretroviral therapy including PIs (HAART).3 Here we report that prolonged PI treatment in vivo reduced sensitivity of peripheral blood T cells toward apoptosis in vitro even when plasma viral load levels were not decreased and susceptibility for T-cell activation in these patients was not down-regulated.

    “Our observations suggest that the reduced T-cell sensitivity toward CD95-induced apoptosis in vitro might partly explain the observation that an increasing number of patients with virological rebound on PI therapy maintain stable CD4 counts and do not experience clinical deterioration as fast as one could expect from the increased viral load.

    xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx

    “http://www.thebody.com

    Treatment Action Group
    Antiretroviral Horizon: 35th Interscience Conference
    Unveils Results from Several
    Important Clinical Studies
    Protease and paradox

    November 1995

    Saquinavir (Invirase )
    Ann Collier of the University of Washington presented long-term follow-up data from ACTG 229, the 302-patient study which compared AZT+ddC to AZT+saquinavir to AZT+ddC+saquinavir. She showed that while throughout the first six months there were greater CD4 and viral load changes in the the triple-therapy arm compared to the two double-drug arms, clinically the three groups fared the same. [Yet another nail in the surrogate marker coffin.] ”
    “Jonathon Schapiro of Stanford presented an open-label study of two higher doses of saquinavir. Twenty patients each were randomized to receive 3,600 or 7,200 mg saquinavir daily for 24 weeks. Mild liver function test elevations, confusion and gastrointestinal upset were reported at the 7,200 mg dose. CD4 counts rose by an average of 72 cells/mm3 at 4 weeks and by 121 cells at 20 weeks. Thirteen of the forty patients developed either the 48 or 90 mutation over the course of the study; suggesting, but not proving, that the higher doses delay the emergence of resistance. (In a European study of regular dose saquinavir, 50% show low level resistance at week 25, and the rest develop it by week 52.) Curiously though, while the resistance-conferring mutations did not emerge until week 20, plasma HIV-RNA levels bottomed out and began to rebound after only 4 weeks of high-dose saquinavir therapy.”

    Caution !

    A higher CD$4 count does not always pridict increased survival.

    http://www.duesberg.com

    A Ray Of Hope
    Transcript UK BBC Documentary
    Panorama London, March 1996

    Retrovir, the drug better known as AZT, is a billion pound success for a British drug company. But can it do more harm than good? Tonight, Panorama reports on the controversial drug sold as a ray of hope.

    .

    Prof. Weller: “It was important therefore to at least run a trial for several years to get handle on whether it actually did any good in the long term in people that were well.”

    The company in line with some other experts also wanted to rely on a more immediate measure. AZT’s effect on patients’ blood. In particular their number of CD4 blood cells thought vital to the strength of the immune system. The study’s British Chairman rejected this, believing AZT might artificially raise this blood count, without bringing any real health benefit.

    Prof. David Warrell: “We were worried that the CD4 count might be a cosmetic measure.”

    Reporter: “Why then would the company want to include a CD4 count?”

    Prof. Warrell: “Well a CD4 count had the great advantage that the changes were seen early on. Clearly the longer the study the more expensive, the more delayed the results.”

    In fact it looked worse. The figures showed that more patients died among those who took AZT early. 96 died taking it early, 76 taking it late. But the investigators were cautious and anxious to avoid causing alarm. They calculated that given the size of their samples of patients the difference in death rates could be due to chance. It was not statistically significant.

    Dr. Tim Peto: “We were very concerned indeed to avoid scaremongering and statistically that 96 is the same as 76 even though mathematically they’re different.”

    Reporter: “But in fact the result was the wrong way?”

    Dr. Peto: “The result were certainly the wrong way mathematically yes.”

    There was also a paradox. While it did not improve survival, taking AZT early did raise the level of patients’ CD4 blood cells. So it should in theory give them longer life. But it didn’t.

    Prof. David Warrell: “It did seem to be a surrogate marker of potentially misleading index.”

    Reporter: “But this was one of the markers which the company had relied on in its own trial of AZT.”

    Prof. Warrell: “Exactly, so we felt vindicated in our reserve or scepticism about what one could infer from the CD4 count alone.”

    The Concorde doctors had agreed to publish a quick summary of their initial findings. But as Wellcome still maintained the value of CD4 counts this led to further disagreement still maintained the value of CD4 counts this led to further disagreement. The Committee Chairman tried to agree a form of words with the company to go as a letter in The Lancet.

    Prof. Warrell: “The company representatives wanted to tone down the wording of the letter. As the publication data approached the telephone communication was more and more frequent and more and more frenzied, and it really almost degenerated into a matter of considering individual adjectives. We wanted to say the results casts serious doubt on the value of using changes in CD4 counts. A serious doubt. The company were very keen that we should delete ‘serious’, so we deleted ‘serious’ under pressure from the company.”

    A week after the first Concorde results the letter appeared in The Lancet in April 1993.

    Newsman: “British drug company Wellcome has made millions selling AZT and today its shares fell over 15 pence or 7% of the company’s value.”

    AZT came under attack from patients in Britain whose hopes had been dashed.

    Pascal de Bock: “Initially I took the whole box of my tablets and put them in the bin and I mean well all the side effects disappeared. Somehow I wanted to make the wider public know that there was something, a very darker side into that marvellous treatment to help those people who suffer so much. Then suddenly the Concorde trial results just appeared and I felt really ecstatic. It was absolutely marvellous for me to realise that what the decision that I had made without somehow any medical advice had been the right one to make.”

    But the Wellcome Foundation seemed less ecstatic. Four days after the Concorde results at its London headquarters the company briefed the press and city analysts like Peter Cartwright about the trial’s findings.

    Peter Cartwright: “It wasn’t the sort of meeting where maybe its been laid on for months in advance and its well scripted and well rehearsed and comes across as a very slick and very professional affair. This one was damage limitation and called at short notice and the company were on the back foot a little bit.”

    Reporter: “Why do you call it damage limitation?”

    Cartwright: “Well because the share price was falling very rapidly.”

    The company told the press that an adequate analysis of Concorde would show it to fit their own shorter term studies suggesting that early treatment can improve survival. But this was the exact opposite of what Concorde had found. One of the company’s overhead slides shown to the press contradicted another Concorde finding, saying survival appears to be correlated with CD4 response.

    Prof. Ian Weller: “If anything Concorde showed that there wasn’t a correlation between CD4 and survival, so the whole exercise and its a personal view, was one of damage limitation.”

    Reporter: “Was it a distortion of your findings?”

    Prof. Weller: “I think you could interpret some of the overheads as a distortion of the conclusion, the main result, the bottom line of Concorde.”

    Prof. David Warrell: “Both the Chairmen of the co-ordinating committee were outraged by this behaviour of the Wellcome Foundation. I composed a letter and sent it to the Wellcome protesting the misleading information provided at the city meeting.”

    Reporter: “Did you get a response?”

    Prof. Warrell: “We didn’t.”

    Panorama wanted to ask Wellcome staff about their comments to analysts and the press. Dr. Trevor Jones, then Director of Research, and Dr. Paul Fiddian a member of the Concorde team – they both declined to be interviewed.

    Later that year, in December 1993, the whole Concorde team met in a hotel at Paris Airport to approve the wording of their full report. There were disagreements on points of scientifical detail, and one overriding problem.

    Prof. Weller: “Although there were lots of discussions about small points and indeed we did accommodate some of the suggestions, trying to work together on it, the real thing was the last sentence of the paper, and that was the result of this study do not encourage the early use of AZT.”

    In a compromise with the company this conclusion had been left out of the first letter in The Lancet. Now Wellcome wanted to delete it from the full report too.

    Prof. Warrell: “Really it was the conclusion, the main conclusion that they couldn’t swallow.”

    Reporter: “Why couldn’t they swallow it?”

    Prof. Warrel: “Well why means why scientifically or why commercially, I mean why commercially because this would decrease the market of one of their best selling drugs. Why scientifically we could never really understand.”

    Reporter: “There was deadlock. The Wellcome representatives continued to insist on deleting this sentence.”

    Prof. Warrell: “I must say we were a great deal more obstinate this time than we were over the letter because of our experience of the letter. There was no certainty at all that had we compromised the company would not have reneged again after publication.”

    Prof. Weller: “The company rehearsed its criticisms again and then late on in the meeting stated that they felt they couldn’t endorse the report.”

    Panorama wanted to ask why, but Dr. Thierry Nebout and Dr. Jane Yeo the two Wellcome scientists at the meeting have declined to be interviewed.

  172. james Says:

    I dont know if Mr Christopher Nobel is still reading this thread, but if you are I just wanted to thank you for your kind ,co operative , positive comments on another site , I wanted to reply but the “moderator” ended the discussion.

    Also please pass on my regards and thanks to Nicholas Bennett .

  173. james Says:

    “). In particular, it has been suggested that changes of mitochondrial membrane potential ()2 play a key role in apoptotic cascade. Given the important role of apoptosis in the pathogenesis and progression of HIV infection, several studies have specifically focused on apoptosis mechanisms in both HIV-infected and uninfected CD4+ cells (4, 5). In particular, a major role of the mitochondria in the process of CD4 T cell death has been suggested (6, 7). In fact, the reduction of CD4+ cell loss by apoptosis has been considered to be an important aspect of immune reconstitution under highly active antiretroviral therapy (HAART) (8, 9). This is a clinical approach that involves, among others, drugs of different nature, such as HIV reverse-transcriptase inhibitors, e.g., zidovudine (AZT), and HIV protease inhibitors (PIs). Those most commonly used are nelfinavir, indinavir (ind), saquinavir (saq), and, very recently, lopinavir (lop). Their “combined activity leads to viral load lowering as well as to reduced cell loss. Several lines of evidence have schematically indicated that AZT may be an apoptotic inducer (10), while PIs can be considered as apoptosis-hindering drugs (9, 11, 12). More specifically, the use of AZT, although of relevance in the control of the progression of the disease through direct activity on viral replication, was demonstrated to be per se cytotoxic to the immune system cells (13). In particular, some studies clearly indicated that AZT was irreversibly incorporated into mitochondrial DNA inducing
    mitochondrial dysfunction by acting on polymerase and inhibiting oxidative phosphorylation (14, 15). This resulted in apoptotic cell death process (10, 15). In contrast, some in vitro and ex vivo studies suggested that PIs, independent from any viral infection, were able to inhibit PBMC loss and to restore impaired T cell proliferative response (16). Accordingly, apoptotic cell death of both HIV-infected and uninfected cells was apparently inhibited”

    Activated cells

    In contrast, results obtained in activated human lymphocytes (Fig. 1B) were the following: 1) apoptotic proneness of activated lymphocytes was significantly higher compared with resting cells, and 2) receptor-mediated stimuli (TNF-, TRAIL, anti-Fas) were characterized by lower values of apoptosis (54, 22, and 34%, respectively) compared with radiation (>80%); more importantly, 3) a significant decrease in cell loss by apoptosis was found in activated human T lymphocytes pre-exposed to PIs before exposure to various apoptotic inducers (Fig. 1B). In particular: 1) the protection conferred by PIs (ind, saq, and lop, 100 nM) was, regardless of the stimulus used, significant in receptor-mediated (anti-Fas, TNF-, TRAIL) as well as in receptor-independent (UVB and UVB + anti-CD95/Fas-neutralizing Ab) apoptosis, and 2) no significant difference was found between various PIs in terms of antiapoptotic activity. Specifically, the mean values obtained from quantitative cytofluorometric analysis (conducted by pooling together the results obtained with ind, saq, and lop) indicated that PIs were capable of significantly reducing TNF—mediated apoptosis (-70.1 ± 7%), Fas-mediated apoptosis (-55.4 ± 8%), TRAIL-induced apoptosis (-49.0 ± 6%), and UVB-mediated apoptosis (-79.6 ± 8%) in activated T cells. In Fig. 1, only the results obtained with ind and saq have been reported.

    “Because mitochondria hyperpolarization has been related to ROI hyperproduction (29), quantitative analysis of ROI generated during lymphocyte activation in the presence or absence of various PIs (saq, ind, and lop) was also performed by flow cytometry. In Fig. 3B, the increased ROI production detected using DHR 123 in activated T cells compared with resting cells can be observed (compare resting and IL-2/PHA dot plots and histograms). In particular, this increased ROI production was overall detected in a subset of lymphocytes that increased their physical parameters, i.e., their volume (dot plots, R2 region), as detected by fluorescence intensity histograms (green lines). Importantly, PI drugs, e.g., lop, were capable of significantly hindering both ROI production (green lines, see median values in the histograms) and changes in physical parameters described above and detectable in activated T lymphocytes (dot plots, R2 region). Hence, PIs (saq, ind, and lop) were able to significantly prevent either mitochondria hyperpolarization (Fig. 3A) or oxidative imbalance (Fig. 3B) associated with IL-2/PHA activation. Only data obtained with lop, considered as representative results, are shown in Fig. 3.”

    “Effects of PIs on AZT subcellular activity

    Previous reports suggested that one of the most important drugs in the management of AIDS, i.e., AZT, can be considered an apoptotic inducer in activated lymphocytes (10). More interestingly, it was also suggested that mitochondria could represent an important intracellular target of this drug (34, 35, 36, 37). We thus decided to evaluate whether mitochondrial toxicity and subsequent apoptosis induced by AZT could be counteracted by PI subcellular activity. We used AZT as mitochondriotropic drug and apoptotic inducer in untreated or PI-treated IL-2/PHA-activated lymphocytes. Results reported in Fig. 4, A and B (because no significant differences were detected among various PIs, only representative results obtained with ind are shown), clearly showed that: 1) PIs prevented AZT-induced apoptosis (Fig. 4A) and 2) this protection was mediated by a protective effect exerted on mitochondrial homeostasis (Fig. 4B, left panels, III quadrant). In addition, our results also show that: 3) AZT sensitized lymphocytes to receptor-mediated apoptotic triggering, e.g., by anti-Fas (Fig. 4A) and that 4) this sensitization was paralleled by an increase in the percentage of cells with depolarized mitochondria (Fig. 4B, right panels). Overall, these findings suggest that: 1) AZT-induced mitochondrial-mediated cell death of activated lymphocytes can be significantly prevented by PIs (the mean decrease of apoptosis exerted by PIs was 74 ± 12%, pooling results from saq, ind, and lop) (Fig. 4A); 2) the percentage of cells with depolarized mitochondria can be significantly lowered by pretreatment with PIs (data obtained by using saq, ind, and lop pooled together showed a mean decrease of 68 ± 8%) (Fig. 4B); 3) a significant correlation exists between the two events (r = 0.978, p < 0.001); and, finally, 4) cumulative synergic proapoptotic effects of AZT and various proapoptotic stimuli, e.g., by anti-Fas (Fig. 4A), can be counteracted by different PIs. In Fig. 4, A and B, considering the similar behavior exerted by PIs toward various apoptotic stimuli, only the more extensively studied physiologic stimulus, i.e., anti-Fas, is shown.

    Plus AZT depletes intracellular glutathione, induces cell death, mitochondrial damage, P.I.’s reduce this oxidative effect of AZT , P.I. based “haart” has been shown to increase intracellular GSH, plasma vitamin c and vit e levels as well as reduce apoptosis induced by oxidizers like radiation, AZT,Morphine,hydrogen peroxide.

    Like antioxidants do with the above plus other oxidizers like crystal meths which depletes/makes? cd4 dissapear/migrate after all we measure only the blood that has 2% of the t cell populaton in redicence temporily.

    Lancet Oncol. 2003 Sep;4(9):537-47.
    Use of HIV protease inhibitors to block Kaposi’s sarcoma and tumour growth.

    Sgadari C, Monini P, Barillari G, Ensoli B.

    Senior Investigators at the Laboratory of Virology, Istituto Superiore di Sanita, Rome, Italy.

    HIV protease inhibitors are antiretroviral drugs that block the enzyme required for production of infectious viral particles. Although these agents have been designed to selectively bind to the catalytic site of HIV protease, evidence indicates that other cellular and microbial enzymes and pathways are also affected. It has been reported that patients treated with highly active anti-retroviral therapy (HAART) containing a protease inhibitor may be at reduced risk of Kaposi’s sarcoma (KS) and some types of non-Hodgkin lymphomas; some disease regressions have also been described. Here we review recent data showing that several widely used protease inhibitors, including indinavir, saquinavir, ritonavir, and nelfinavir, can affect important cellular and tissue processes such as angiogenesis, tumour growth and invasion, inflammation, antigen processing and presentation, cell survival, and tissue remodelling. Most of these non-HIV-related effects of protease inhibitors are due to inhibition of cell invasion and matrix metalloprotease activity, or modulation of the cell proteasome and NFkappaB. These elements are required for development of most tumours. Thus, by direct and indirect activities, protease inhibitors can simultaneously block several pathways involved in tumour growth, invasion, and metastasis. These findings indicate that protease inhibitors can be exploited for the therapy of KS and other tumours that occur in both HIV-infected and non-infected individuals. A multicentre phase II clinical trial with indinavir in non-HIV-associated KS is about to start in Italy.

    Publication Types:
    Review

    PMID: 12965274 [PubMed – indexed for MEDLINE]

    xxxxxxxxxxx

    Drug Resist Updat. 2003 Aug;6(4):173-81.

    HIV protease inhibitors as new treatment options for Kaposi’s sarcoma.

    Barillari G, Sgadari C, Toschi E, Monini P, Ensoli B.

    Laboratory of Virology, Istituto Superiore di Sanita, V.le Regina Elena, 299, 00161 Rome, Italy.

    A reduced incidence and regression of Kaposi’s sarcoma (KS) and other tumours has been reported in Acquired Immune Deficiency Syndrome (AIDS) patients treated with antiretroviral combination therapies containing Human Immunodeficiency Virus (HIV) protease inhibitors (PIs) such as indinavir or saquinavir. Indeed, evidence indicates that although PIs were designed to selectively inhibit the HIV protease activity, they can interfere with several cellular pathways and can inhibit tumour growth. In particular, our recent results indicate that doses of indinavir or saquinavir similar to those employed to treat AIDS patients can induce regression of experimental KS by directly blocking two fundamental steps of KS initiation and progression: new blood vessel formation (angiogenesis) and KS tumour cell invasion. This is because indinavir or saquinavir inhibit the activation of matrix metalloproteinase-2 (MMP-2), a basement membrane-degrading enzyme, which is required for the progression of most tumours. Based on these results, a multicentre clinical trial is now starting in Italy, which will assess PI effects on the progression of KS in HIV-uninfected individuals (classical KS).

    Publication Types:
    Evaluation Studies

    PMID: 12962683 [PubMed – indexed for MEDLINE]
    xxxxxxxxxxxxxxxxxxxxxxxxxxxxxx

    Antioxidants NAC and GSH inhibits TB in vitro in humans with “hiv”, selenium defiency (involved in GSH production) in drug users predicts 13 fold liklyood of TB. crystal meths increases “fiv” 15 fold it oxidizers, it depletes GSH , it induces cell death/apoptosis and acetyl l carnitine (raises gsh amognst others things like mitochondria) and NAC a pro GSH agent block /reduce apoptosis induced by crystal meths, heroine and other recreational drugs /medical drugs “arv’s”/chemo’s.

    Also these agents could reduce and delay the need for more expensive and toxic “arv’s” which aslo have broad spectrum antimicrobial effects against many if not all the “O.Is” that are sometimes called “aids”.

    Antioxidants can also be used if “arv” treatment is need, they can be used along side and when they are there is very good evidence that negative/side effects/toxicity/ozidation can be reduced by combinations of antioxidants , micro nutrients ect and that these agents an also increase the positive effects of “arv’s”.

  174. james Says:

    Nac NIH/NCI 2001 study reverses established KS in vivo model and doubles the life span. Ks occurs in the absence of “aquired immune defiency” i is not caused by either hhv-8 or immune suppression low cd4.

    Whats really crazy about all in this artical this is that sadley the artical does not get the “hiv” protease inhibitors have there anti KS effects regardless of “viral” presence or non presence. Even with “viral” rebound “drug resistance” as already shown PI’s have the anti apoptosis effects independant of “viral” presence or non presence. And of course independant of “CD4” levels LOL.

    I hope you dont mind but I would like to repost the previouse two references about “hiv” specific LOL protease inhibitors treating non “hiv” kaposi Sarcoma in vitro and invivo and now trialed in humans. I would like to post them in the KS not aids post on here becusause they belong there as well, these two post are interlinked because others and I hypothesise the “hiv” P.I.’s act like antioxidants sometimes interefering with apoptosis/cell death INDEPENDANT of “viral” presence or not particulary so with activated t cells.

    PPPPPPSSSSSSSSSSSSTTTTTTTTT
    REMEMBER NAC INHIBITS?REVERSES KS IN VIVO< WELL P.I’S RAISE GSH AS WELL AS REDUCING OXIDATIVE STMULI JUST LIKE NAC DOES.

    xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
    http://www.thebody.com/catie/switch_ks.html

    Canadian AIDS Treatment Information Exchange
    French Doctors Suggest That Therapy Switch May Cause KS Relapse

    By Sean R. Hosein

    July 8, 2003

    Kaposi’s sarcoma (KS) is a tumour that usually appears on the skin and most commonly affects gay and bisexual men with HIV/AIDS. KS was more common in North America and Western Europe at the beginning of the AIDS epidemic than it is now. Although KS most commonly affects the skin, over time, as immunity weakens, KS tumours can develop inside the body, particularly near lymph nodes and the digestive tract and in mucous membranes such as the mouth. As the tumours grow they can block lymph vessels, causing fluid to build up, which results in discomfort, further complications and even death. Treatments available for KS include radiation and chemotherapy, but these have seldom resulted in a cure for KS in people with HIV/AIDS (PHAs).
    In the mid-to-late 1990s, protease inhibitors (PIs) became widely available in high-income countries. When used as part of combination therapy, PIs helped put KS into remission. Researchers suspected that this occurred because PI combination therapy raised CD4+ cell counts and reduced levels of HIV in the blood. The changes in cell counts and viral load allowed the immune system a chance to begin repairing itself and perhaps to better fight KS tumours.

    However, this theory may now have to be reexamined, based on new findings from Paris, France. There, doctors reported that five PHAs who switched from a PI-based regimen to a regimen based on non-nukes (NNRTIs), such as efavirenz (Sustiva, Stocrin) or nevirapine (Viramune), had relapses in their KS.

    PI Therapy
    At the time the PHAs were originally diagnosed with KS, all five had “widespread” skin tumours. They received chemotherapy and/or radiation therapy. Eventually they took PI-based combination therapy for about 2½ years, and their KS went into remission and cleared up. However, three of the PHAs’ therapy was eventually unable to suppress HIV levels; the remaining two wanted simpler regimens. So doctors changed their combinations to ones based on non-nukes instead of PIs.

    After the Switch
    On average, the KS relapsed one year after the PHAs switched from PIs to a non-nuke. At the time the relapse occurred, in four of the five PHAs, CD4+ cell counts were relatively high — ranging between 350 and 1,300 cells. Also, in four of the five PHAs, viral loads were low — fewer than 20 copies.

    PIs and KS
    The doctors note that the recurrence of KS in their patients cannot be explained by low CD4+ counts or high viral loads. In seeking other explanations, the doctors report certain results of test-tube and animal experiments done by researchers. In these experiments, PIs seem to prevent the growth and development of KS tumours. The drugs appear to do this by blocking the production of growth factors (chemical messengers) needed by KS cells. Moreover, exposure to PIs caused KS cells to die.

    The report by the French doctors about KS relapse is interesting. However, much more study and analysis is needed to confirm these findings in other PHAs as well as to reconcile them with results from other clinical trials where combination therapy with either PIs or NNRTIs resulted in the regression of KS.

    In the meantime, the French doctors warn that other doctors should use caution when switching their patients who previously had KS from a PI to an NNRTI.

    References
    Sgadari C, Barillari G, Toschi E, et al. HIV protease inhibitors are potent anti-angiogenic molecules and promote regression of Kaposi sarcoma. Nature Medicine 2002; 8(3):225-232.
    Gaedicke S, Firat-Geier E, Constantiniu O, et al. Anti-tumor effect of the human immunodeficiency virus protease inhibitor ritonavir: induction of tumor-cell apoptosis associated with perturbation of proteasomal proteolysis. Cancer Research 2002; 62(23):6901-6908.
    Bani-Sadr F, Fournier S and Molina JM. Relapse of Kaposi’s sarcoma in HIV-infected patients switching from a protease inhibitor to a non-nucleoside reverse transcriptase inhibitor-based highly active antiretroviral therapy regimen. AIDS 2003;17(10):1580-1581.
    Gill J, Bourboulia D, Wilkinson J, et al. Prospective study of the effects of antiretroviral therapy on Kaposi’s sarcoma-associated herpes virus infection in patients with and without Kaposi’s sarcoma. Journal of Acquired Immune Deficiency Syndromes 2002;31(4):384-390.

  175. Gene Semon Says:

    From Robert Houston:

    Drs. Benigno Rodriquez and Michael Lederman, sing paeans of tribute to the sacred doctrine in terms bordering on religious fanaticism (e.g., “There is absolutely no doubt that HIV is the cause of AIDS”). But heretofore the tacit or even explicit corollary has been to the effect that “there are no other causes or influences worth mentioning,” i.e., “thou shalt worship no other gods.” At the very end, however, the authors append a summary that seems like a plea to let a thousand flowers bloom. They conclude:

    “Levels of HIV in blood explain only a small portion of the variability in the rate at which CD4 T cells are lost. Therefore… Expanded efforts to identify the other elements that drive CD4 cell losses in chronic HIV infection are needed.”

    Again, thanks for the clarity, Robert Houston. Here we see the JAMA RNA/CD4 authors exhibit the appropriate ritualistic behaviours to maintain their continued funding AND proceeding in a scientific manner with a comment that moves the discussion forward.

    Additionally, the comments by rethinker James display our non-monomania (!?) – and how much poor Chris is in over his head – , i.e. evaluating the use of pharma drugs when appropriate models indicate their efficacy.

    I feel sorry for Chris N because he doesn’t get what’s going on. At this point, any reasoning, literate person can see the unsatifactory performance of the surrogates pol or gag RNA that “explain only a small portion of the variability in the rate at which (surrogate for AIDS)* CD4 cells are lost” based on the single virus causing single disease epidemic model. *(parens added)

    When one decides, based on this poor performance, to revisit biological plausibility, strength of the association – i.e marker, not the agent itself – , etc. and concludes that reorderings of the identified risk factors/diseases/treatments (e.g. James above), in the collective phenomena known as AIDS, are necessary for progress; that person must have a psychiatric disorder. Of course.

    I am taking Chris’ advice and submitting to the DSM IV a new disease, “failure to take instructions from the established authorities in science: autocognitive-mania”. In a falsification process known as the Catch 22 Effect, if they respond, “you’re crazy”, I’ll know that I’m sane.

  176. nohivmeds Says:

    Just a quick note — while reading through some sites for HIV+ folk last night, I saw (yet again) the author of a “guide” to viral load say that it measures “viremia.” Disgusting, really, the lies that are told with such convincing sounding scientific language, to those who actually need to know the truth.

  177. CarefulObserver Says:

    Noble said,

    “Honestly the arrogance of people like you that think they can interpret papers better than the authors is astounding.”

    Yeah, kind of like you do with Duesberg, huh, Chris??

  178. james Says:

    http://www.altheal.org
    taken from above and below
    http://www.aidsmythexposed.com general section thread titled viral-load doesnt predict cd4

    You might want to read this statement by Rodriguez (JAMA: viral load) and Lederman:

    http://www.aidstruth.org/rodriguez-lederman.php

    “There is absolutely no doubt that HIV is the cause of AIDS.”

    “Our results imply that although HIV infection drives the progressive immune deficiency of AIDS (as evidenced by the response to successful treatment with anti-HIV medicines, which decrease the viral load, increase CD4 cell numbers, and prevent or help resolve opportunistic infections, reflecting an improvement in immune function), there must be other intervening elements that cause progressive CD4 cell losses in HIV infection.”

    Copy and paste url
    http://groups.msn.com/AIDSMythExposed/ general.msnw?

    action=get_message&mview=0&ID_ Message=25593&Last Modified= 4675595679954333234

    BHIVA: One-in-three UK HIV deaths ‘not directly related to HIV’
    http://www.aidsmap.com/en/news/ 8DB0098A-5707-4F4C-84FA-AE 9C854865F6.asp
    One-in-three UK HIV deaths ‘not directly related to HIV’

    From: MrChristopher (Original Message) Sent: 18/10/2006 18:16
    I saw this this morning.

    One-in-three UK HIV deaths ‘not directly related to HIV’

    “One-in-three deaths that occurred in HIV-positive individuals in the United Kingdom between 2004 and 2005 were not directly related to HIV”

    and;

    “CD4 and viral loads in the last six months of life were not uniformly poor. In fact, around half of all people who died had CD4 cell counts above 200 cells/mm3 and 30% had ‘undetectable’ viral loads. Consistent with these data is the finding that one-third of deaths were not considered to be directly linked to HIV infection.”

    Wow, they really try and squirm out of this uncomfortable information by saying ‘consistent with these data is the finding that one-third of deaths were not considered to be directly linked to HIV infection’.

    Unfortunately they didn’t tell us who did and did not have ‘poor’ stats ‘consistent’ with the ‘HIV’ paradigm. Meaning the article talks about this 1/3 of deaths in ‘HIV’ positive people whose deaths are not attributed to ‘HIV’. And then they say a big bunch of the total deaths in 2004-2005 had CD4 counts above 200 (though they didn’t give the range) or had ‘undetectable’ viral loads. They then try and imply these people with ‘non-standard’ surrogate markers were the ones that did NOT die from ‘HIV’. It’s squirmy language.

    It’s also funny how they say, ‘CD4 and viral loads in the last six months of life were not uniformly poor’

    What they COULD have said is, the surrogate markers for half the deaths didn’t fit the ‘HIV” paradigm.

    Chris
    Co-moderator

    First Previous 2-8 of 8 Next Last

    Reply
    Recommend (1 recommendation so far) Message 2 of 8 in Discussion

    From: HansSelyeWasCorrect Sent: 19/10/2006 17:56
    Also worthy of note:

    “4 due to accidental injection drug overdose (1.0%)”

    Now out of 133 adults in the general population of the UK, how many will die of this? Not even close to 1. Therefore, many of these “AIDS patients” are likely serious drug abusers, perhaps an overwhelming majority. Then there were the anal and penile cancer deaths. Again, what are the chances of someone dying of these, especially at the ages that these people likely were at the time? The “Hep B/C” deaths are also clearly related to this, because the liver is the “detox” organ. When will they ever remove the “HIV” colored glasses they are wearing?

    Reply
    Recommend Message 3 of 8 in Discussion

    From: HansSelyeWasCorrect Sent: 19/10/2006 20:48
    Looks like it was 389 adults, not 133. Still is an incredibly high incidence of these uncommon afflictions.

    Reply
    Recommend Message 4 of 8 in Discussion

    From: straightguyantiauthority Sent: 20/10/2006 13:42
    LOVE the “HIV colored glasses” expression

    A great metaphor for future use in getting people to reevaluate the data.

    Reply
    Recommend Message 5 of 8 in Discussion

    From: HansSelyeWasCorrect Sent: 20/10/2006 18:15
    I was thinking of the picture of Ho on the cover of Time (when he was “man of the year”). At least his glasses were pretty.

    🙂

    Reply
    Recommend Message 6 of 8 in Discussion

    From: GlutathioneSurvival1 Sent: 30/10/2006 01:20
    This “cd4” and “viral-load” is so so bollox, I cant see how doctors and “scientist” can have such tunnle vision and blinkers over there eyes, I had two friends in two weeks both with “undetectable” “viral-loads” and “cd4” around 700 with “PCP” an “aids” or rather in the west THE “aids” defining disease but theres no “virus” there and no “aquired immune defiency” -low “cd4” or anywhere near low “cd4” how can they just carry on ignoring, turning a blind eye, or not asking or thinking theres something very wrong with this theory. But no they stumble across these cases all the time, then just pick themselfs back up and forget, ignore these cases and carry on with the holy “hiv” “aquired immune defiency”=low “cd4” mantra of “aids” the new unquestionable “god” of “science” now run by religious zealots.

    Very interesting post Mr Christopher and guys thanks.

    Best wishes

    Hugs

    james

  179. Otis Says:

    The Final Nail in the Rodriguez/JAMA Coffin

  180. Chris Noble Says:

    The only thing that this “nail” proves is that Dr Dach can’t draw a line in the middle of a distribution.

    Rodriguez et al provide the median CD4+ depletion rate for each HIV viral load group on the figures.

    -37.3
    -42.8
    -45.8
    -48.9
    -52.2

    The “center bars” that Dr Dach hand draws on the figure do not correspond to these figures.

    Visual inspection of the figures also shows that the “center bars” are not in the centre of the distribution.

    In the top graph there is far more black ink to the right of the “center line” and in the bottom graph there is far more black ink to he left of the “center bar”.

    I have repeatedly asked Dr Dach to provide a description of the mathematical methods that he used to calculate his “center bars”. He hasn’t answered. Most people conclude that he simply used wishful thinking.

    HIV “rethinkers” are going to incredible lengths to avoid admitting that the study found that on average people with high HIV viral load had a faster CD4+ cell depletion rate than those with a low HIV viral load.

    Dr Dach’s “center bars” are only evidence of his own dishonesty.

    Why other HIV “rethinkers” with mathematical training tolerate this nonsense is bewildering.

  181. pat Says:

    Chris,

    I am having a very hard time believing anything you say and not because I think you are better at disseminating the medical literature but merely because of your style of argument. I find your style dismissive, arrogant and patronizing and I find myself wondering what it is that motivates you to appear day after day to engage the holders of opposite view points with such disdain. Ever since I started harbouring my own questions about the official story behind HIV and bumping into a rather well organized and vocal dissent, I have naturally been following it closely.
    From a purely presentational point of view, the “rethinkers” take the gold both for style and clarity. I hear them accused of peddling their “pseudo-science” to lay audiences by writing books and blogs, appearing on radio and God-knows-what else “cheap-shot”. How else would they do it to get their message out considering the very restrictive and venimous environment these people find themselves in, as is clearly demonstrated by yours and the “mainstream”s dismissive, arrogant and patronizing tone. For an example of the “either you are with us or you are against us” world
    visit some of the links posted to the right of this column. AidsTruth.org is the single most insulting message I have yet come across in this entire AIDS Info War. It is you and the likes of Moore that unabashedly peddle a theory by declaration and offering NOTHING by way of substance or information. My definition of peddling.

    You say:
    “Visual inspection of the figures also shows that the “center bars” are not in the centre of the distribution.

    In the top graph there is far more black ink to the right of the “center line” and in the bottom graph there is far more black ink to he left of the “center bar”.

    Are you having an artistic problem with the line or is there another meaning to this “more ink” thing but, true to style, you explain it away with a personal dismisal:
    “Dr Dach’s “center bars” are only evidence of his own dishonesty.”
    This doesn’t explain anything. AidsTruth doesn’t explain anything. Have I simply been convinced to believe in a fatamorgana because rethinkers are better manipulators?
    I have now seriously come to doubt the official relationship between HIV and AIDS because of the absurdity of the arguments and the scorch and burn tactics of the science. Duesberg was and is still correct on this point too. We are trying to kill a rabitt with a nuclear bomb. Observations, conclusions, “Overwhealming truths” and disclaimers and character assassinations in such obvious conflict I am surprised my screen isn’t in flames.

    “Dr Dach’s “center bars” are only evidence of his own dishonesty”.

    Dach is now just another of a long list of people who have been accused of dishonesty by you but have failed to convince anyone of it.What IS IT he is being dishonest about? The choice of black ink? What is it these people are being dishonest for anyway? What is the gain? WHO HAS MOST TO GAIN? What is YOUR gain?

    PS: try this, “Every statement accurate except where irony intended.” My grand father used to say “whatever you do, don’t panic”
    also meaning: “A gentleman doesn’t loose his shit”.
    What is YOUR gain out of slinging shit? My gain is zilch, nada.

  182. Chris Noble Says:

    Are you having an artistic problem with the line or is there another meaning to this “more ink” thing but, true to style, you explain it away with a personal dismisal:

    Dr Dach’s patented “center bars” are supposed to be in the centre of the distribution. I assume he means the median which has a strict meaning in statistics. The median is the value for which 50% of the distribution is below it and 50% is above. In a non-technical description there should be the same amount of black ink to the left and to the right of the median. This is clearly not true as anyone can see. In the top graph the value for the median is actually given as -37.3 yet Dr Dach has drawn his “center bar” at about -50.

    Dr Dach was obviously trying to prove something with his “center bars” so it was a natural question to ask what these “center bars” represented mathematically. Dr Dach has failed to respond. Perhaps initially Dr Dach’s statistical nonsense could be explained by ignorance.

    Now the only answer that I can think of is that Dr Dach is simply being dishonest.

  183. YossariansGhostbuster Says:

    To which one might add, Dr. Dach will not be answering as in

    “Comments to this post are closed.” cf Otis

  184. Truthseeker Says:

    This does not mean that Comments here are closed, of course. The policy of this blog is to expose all arguments for the supernatural qualities of HIV to daylight and reveal them as they are, and make them available for prolonged examination for those who cannot see their quality immediately.

    After all, the chief responsibility for the HIV∫AIDS debacle lies with those who have blatantly censored the review which would have otherwise have despatched the paradigm in short order, or about as fast as a direct hit with Combat despatches a group of roaches.

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