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How Gallo proved that HIV was not the cause of AIDS


His original paper’s result ignored by the world for twenty years

Robert Gallo‘s recent letter to Harper’s, just published in the May issue (see previous post), provoked a thought which we thought deserved a post of its own, for the result of checking one of his sentences reminded us of a little known fact: one of his original papers at the beginning of the HIV?AIDS affair in May 1984 had a surprising result which has been long overlooked.

In fact, the press conference at which Margaret Heckler, Heath Secretary of the Reagan administration, presented Gallo as the savior of the day in being about to publish four papers in Science finding HIV was the probable cause of AIDS, appears to have been mistaken.

Contrary to the report typed rather too hastily by Larry Altman for the front page of the New York Times the day after the press conference, the ebullient Bob had actually proved that HIV was almost certainly not the cause of AIDS. In fact, in this helpful result he preceded Peter Duesberg by at least two years in demonstrating that the linkage between HIV and AIDS was unsustainable.

Going back to the Gallo letter in Harper’s, this is why the most remarkable sentence Gallo pens is the one saluting his moment of epiphany when he decided that HIV was the cause of AIDS: “In 1984, when my colleagues and I were first to claim—and in my view demonstrate—the linkage of HIV to AIDS, we showed that we could isolate HIV from forty-eight individuals who had AIDS.”

The bold effrontery will amuse seasoned admirers of the pr genius of HIV?AIDS’s greatest scientist, and not just because in the first place it was Luc Montagnier of the Pasteur who first “linked” HIV to AIDS in a 1983 paper. Luc Montagnier hadn’t claimed that HIV alone could be the cause of AIDS, and he was happy to forward HIV to Robert Gallo on request, and in fact did so twice, since Bob lost the first batch.

Montagnier was not amused when Gallo subsequently claimed to have discovered it all by himself, however, and after an extended international wrangle at the governmental level over royalties, which established that Gallo’s virus was in fact Montagnier’s, discovered by Gallo in the two Federal Express packages from France when they arrived at the NIH and the receipts were signed and returned to Montagnier, found he had to share credit for HIV with Gallo as the “co-discoverer”. But that’s another story.

For the paper Gallo is referring to in his letter to Harper’s is “Frequent Detection and Isolation of Cytopathic Retroviruses (HTLV-III) from Patients with AIDS and at Risk for AIDS”, the key paper of four published on May 4, 1984 in Science, which demonstrated that HIV was almost certainly not the cause of AIDS.

How Gallo managed to pass this off so brilliantly at a press conference before it was published, as suggesting so powerfully that HIV was the cause of AIDS that the celebrated Larry Altman of the Times reported that inverted conclusion the next day, is a puzzle that science historians have yet to solve. We put it down to the fact that Larry was in a hurry to get his story on the front page, and no one ever bothered to read the paper itself once the Times had spoken.

But that paper’s landmark finding is the reason why Gallo is forced to leave the number “forty-eight” standing out there in his letter all by itself, not saying 48 out of how many, because in fact he found the virus in blood from 48 individuals out of 119, and 22 of the 48 did not have AIDS, rather than all of them being “individuals who had AIDS”, as he states above in what must have been a slip of his pen in writing to Harper’s.

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“So the historic irony is that the man who proved that HIV was not the cause of AIDS twenty years ago was Robert Gallo himself. Luckily for him, however, the science of AIDS has been run by press conference ever since, so no one has noticed.”

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In fact, the paper shows that he found virus more often in “pre-AIDS” people without AIDS (18 out of 21, or 86%) than people with AIDS (26 out of 72, or 36%), and he found that it wasn’t able to survive in a dish more than “2 to 3 weeks” in the blood of AIDS patients and “pre-AIDS” patients, while it flourished in established T-cell lines.

“Pre-AIDS” patients were people in a risk group – ie gay in this case – who had developed some chronic swelling of the lymph glands (lymphadenopathy), or some undefined low count of white blood cells (leukopenia). They must have often been in the early stage of HIV infection, before antibodies had mounted sufficiently to erase the infection, as this paper revealed happens in the majority of cases even in people who progress to AIDS.

Clearly, according to the paper, the best way to get rid of HIV is to get AIDS proper, easily achieved by taking large amounts of designer drugs and eating badly. In other words, if you think that HIV is the problem, hurry up and have fun and get AIDS, and you’ll likely get rid of HIV entirely. We are saying no more than the paper says with its data.

Thus the paper suggested not “strong evidence of a causative involvement of the virus in AIDS,” as Gallo wrote at the end of it, but the exact opposite. That is to say, it demonstrated that HIV was almost certainly ruled out as the cause of AIDS, since not only did it flout Koch’s first postulate by being found in only one third of AIDS patients’ blood samples, but it was more likely to be seen in pre-AIDS patients than people with AIDS, in whom it mostly wasn’t found.

So the historic irony is that the man who proved that HIV was not the cause of AIDS twenty years ago was Robert Gallo himself. Luckily for him, however, the science of AIDS has been run by press conference ever since, so no one has noticed.

If a Nobel prize is ever awarded for solving AIDS, however, surely Gallo as well as Peter Duesberg is in line for this honor. For nothing could have been more helpful that to rule out HIV at that early stage in the search for the true solution to defeating the novel outbreak of immune system deficit.

Clearly the real culprits in this gross neglect of Robert Gallo’s initial breakthrough finding are the people, whoever they are, who prevented this original scientist from getting his true message across to the press and public, and instead pressured him to stick with a misunderstanding of his true achievement for over twenty years, at the cost of many lives lost to AZT and current antiviral medications, which his paper showed so long ago are inappropriate, and which we now know have unpleasant side effects involving large humps and dying of liver failure.

Whoever they are, they must have exerted massive pressure on this leading figure in the drama of what was the best reported health disaster of all until bird flu came along. For Bob Gallo is not famous for his reticence. The financial or political interests behind this must have been very large to win this distinguished scientist’s presumably reluctant coperation.

38 Responses to “How Gallo proved that HIV was not the cause of AIDS”

  1. McKiernan Says:

    Truthseeker, you certainly ought be commended for doing an excellent job revising facts to match your bias and providing your readership with some carefully written mis-information. The Gallo article appears to disagree with your conclusions:

    The Abstract says:

    Frequent detection and isolation of cytopathic retroviruses (HTLV-III) from patients with AIDS and at risk for AIDS.

    Gallo RC, Salahuddin SZ, Popovic M, Shearer GM, Kaplan M, Haynes BF, Palker TJ, Redfield R, Oleske J, Safai B, et al.

    Peripheral blood lymphocytes from patients with the acquired immunodeficiency syndrome (AIDS) or with signs or symptoms that frequently precede AIDS (pre-AIDS) were grown in vitro with added T-cell growth factor and assayed for the expression and release of human T-lymphotropic retroviruses (HTLV). Retroviruses belonging to the HTLV family and collectively designated HTLV-III were isolated from a total of 48 subjects including 18 of 21 patients wih pre-AIDS, three of four clinically normal mothers of juveniles with AIDS, 26 of 72 adult and juvenile patients with AIDS, and from one of 22 normal male homosexual subjects. No HTLV-III was detected in or isolated from 115 normal heterosexual subjects. The number of HTLV-III isolates reported here underestimates the true prevalence of the virus since many specimens were received in unsatisfactory condition. Other data show that serum samples from a high proportion of AIDS patients contain antibodies to HTLV-III. That these new isolates are members of the HTLV family but differ from the previous isolates known as HTLV-I and HTLV-II is indicated by their morphological, biological, and immunological characteristics. These results and those reported elsewhere in this issue suggest that HTLV-III may be the primary cause of AIDS.

    So the paper does not say the exact opposite of what you propose. And perhaps your readers will also be appreciate a 1989 report in the Journal of Clinical Microbiology in which:

    Human Immunodeficiency Virus type 1 was Detected in All Seropositive Symptomatic and Asymptomatic Individuals and in None of 131 healthy HIV-1 antibody negative individuals.

    This Abstract says

    We isolated HIV-1 or detected HIV-1 DNA sequences from the PBMC of all 409 HIV-1 antibody-positive individuals. None of 131 healthy HIV-1 antibody-negative individuals were HIV-1 culture positive, nor were HIV-1 DNA sequences detected by PCR in the blood specimens of 43 seronegative individuals.

    The conclusions to those findings, I’m sure will be the subject of discussion in future posts. I would hope that some of your commenters would not think this comment too distal in reference to suggest one cannot get AIDs without hiv.

    Thank you for allowing me to comment.

    Your pal in science, Catch 22 McKiernan

  2. Mark Biernbaum Says:

    McKiernan – what is your HIV status? These days, it seems relevant for that to be disclosed. Everyone in the world knows I’m positive now, cause of Harper’s. I’m always interested in what the status of others is.

  3. McKiernan Says:

    Mark,

    To my knowledge, I am not HIV positive. I have given blood in the past and have not been notified to have any further testing, so I can assume I am HIV negative as the Red Cross
    in my area does check blood donors for HIV and refer them for further evaluation. I work in a clinical setting and follow universal precautions with rubber gloves etc.. for the past 23 years. I have not had any needle sticks from HIV positive patients for whom I occasionally provide care. So there has been to date no need for a formal HIV test either from my work of from a health/medical status.

  4. Truthseeker Says:

    These results and those reported elsewhere in this issue suggest that HTLV-III may be the primary cause of AIDS.

    So the paper does not say the exact opposite of what you propose.”

    McKiernan, thank you for your comment, which demonstrates precisely the point of my post, which is that people are reluctant or unable to read the data in a scientific paper of great simplicity for themselves, but go by what they are told it says, in this case by the author himself in the abstract.

    Yes, Gallo wrote and announced at the press conference that interpretation of the results he had found. But if you read the results for yourself – try it, there is a very easy table in the paper lining up the data – you will see that the paper itself – the CONTENT, the DATA – says the opposite.

    If this is the accuracy with which you understand our posts, and therefore conclude that our position is “biased”, God help you and us. You presumably mean that we are biased towards Duesberg’s views being correct. In fact, we merely recognize that over two decades he has presented a score of reasons to think that HIV is not the cause of AIDS, and has not been answered by a single reason to conclude that he is wrong, except generalized blather about “overwhelming evidence” in non-peer reviewed locales, and that the current drugs work, when it is evident that they reliably ruin your liver and likely end your life (this non-AIDS symptom is the biggest reason for death of AIDS patients right now).

    We are biased, sure. Biased towards good science which is based on good sense, good reasoning and good evidence, as recorded in peer reviewed literature. Robert Gallo’s paper has none of these. It says the opposite of what he says it says. It says that HIV is contraindicated as the cause of AIDS.

    Permit us to say with respect that it is you that are biased, if you call that view, which we based on data quoted from the paper, biased. Since when is it biased to examine a paper carefully and report what its evidence truly indicates, rather than what Robert Gallo likes to say it does?

    The second paper you refer to is like many which later assert that in a study they were able to find virus in everyone who tested positive for antibodies, and unable to find it in those who were negative. In other words their test was 100% accurate, which is not normally claimed, but good for them, and Gallo’s test was inaccurate, since his experience was different.

    But the Gallo paper didn’t note any inaccuracy in his testing, perhaps because it was in vitro and not in vivo. Whatever its accuracy, the fact remains that it found that the presence of HIV virus dropped rather dramatically when pre-AIDS people were compared with those who had progressed to AIDS, and was found in remarkably few of the latter, 26 out of 72, a priori evidence it wasn’t the cause.

    You can argue if you like that his tests were bad at finding virus and if he had used better ones he would have found virus in every sample tested. But what is indicated in all such work is that the amount of virus in patients who are over the initial phase of infection, when antibodies have had time to do their work, is NEGLIGIBLE, and even when people progress to AIDS, it is NEGLIGIBLE, even though the defenses against its proliferation are shot. There is too little in the blood to cause any conceivable problem, short of convoluted imaginary processes as yet undemonstrated. If you find it in everybody with PCR it is because PCR can find a needle in Central Park.

    The fact remains that this was the paper that with three others is the foundation stone of the great $150 billion HIV?AIDS skyscraper in whose rooms people such as yourself work.

    Remove it and one has to ask, what replaces it? Is there a paper which represents better proof that HIV causes AIDS? Not according to the Gallos and Faucis of this world. They are unable to quote any paper that serves as reference for the statement “HIV causes AIDS”, and always have been.

    Therefore one has to ask people such as you, what do you think you are doing, going to work every day in a skyscraper with no foundation? Is this how you want to direct your work with patients who are ill and need effective treatment?

    The $150 billion question for you is this: what do you base your belief in the HIV=AIDS paradigm on? What you are told everyone is basing their work on, what everyone tells you, what every relevant institution’s officials tell you, and what your colleague in AIDS tells you, or what the peer reviewed scientific literature tells you, which none of them seems to read, and which you apparently don’t read yourself, though you pick out the abstract easily enough with Google?

    But if you do rely on the scientific literature, pray tell us, which paper, exactly? It can’t be this one, as we have shown. So which paper or papers is it that you refer to when someone asks you why you believe in the paradigm?

    Or do you just reassure them and yourself that there is “overwhelming” evidence, according to the Durban Declaration, and you have read it in the New York Times?

  5. Robert Houston Says:

    The numbers in the Gallo abstract that McKiernan kindly provided are exactly the same as Truthseeker wrote and show that this post is an accurate representation of Dr. Gallo’s original research. The abstract shows that HIV (HTLV-III) was found in only 26 of 72 AIDS patients (36%) and was absent in 64%. Thus, in accordance with applicable scientific principles, HIV cannot be the cause of AIDS for it abysmally failed Koch’s first postulate: that the proposed pathogen be present in all cases of the disease. This is the fundamental requirement for establishing causation in microbiology.

    It was well known in the early 1980s that AIDS patients had much higher rates of other viral infections, e.g., about 90% for cytomegalovirus and nearly 100% for herpes. The studies through 1984 were based on clinically documented AIDS. Studies after 1985, such as the 1989 study by Jackson et al. that Mckiernan brought up, are not relevant to the question of whether HIV is the culprit. This is because in 1985 the CDC added HIV seropositivity to the definition of AIDS. Thereby, only AIDS patients with evidence of HIV would be counted. In fact, only about 1/8th of the Jackson subjects had AIDS (56 of 409). The fact that sensitive techniques could find traces of virus in those already HIV antibody-positive (2/3rds of whom were completely asymptomatic) tells us nothing about what’s causing AIDS.

    Thank you, Truthseeker, for revealing to the world the truth of Dr. Gallo’s momentous discovery – that HIV is innocent.

  6. McKiernan Says:

    “It was well known in the early 1980s that AIDS patients had much higher rates of other viral infections,”

    Excuse me, but AIDs patients had higher rates of everything . That’s what immune deficiencies do.

    “In fact, only about 1/8th of the Jackson subjects had AIDS (56 of 409).

    Correct. 56 were AIDs diagnosed, 88 were ARC, 265 were asymptomatic. And: “We isolated HIV-1 or detected HIV-1 DNA sequences from the PBMC of all 409 HIV-1 antibody-positive individuals. And: “None of 131 healthy HIV-1 antibody-negative individuals…”

    And from the Gallo study:

    “The number of HTLV-III isolates reported here underestimates the true prevalence of the virus …”

  7. McKiernan Says:

    The $150 billion question for you is this: what do you base your belief in the HIV=AIDS paradigm on?

    With all due respect, McK does not have a $ 150 billion answer, nor does he work in a 150 billion dollar skyscraper. And one suspects McK doesn’t believe in the very paradigm you propose. That of course, you wouldn’t know or even have a real clue. So your response above is functionally aimless and self-servingly defensive. You simply do not know as you have divided the world into them and we or it it those that count and those that don’t count.

    The simple truth is that HIV cannot simply be jettisonned from the AIDs paradigm as some sort of innocent bystander. And until you or others can prove that, that truth will have to stand.

    That Truthseeker is the challenge. Demonstrate to HIV positive people whether ill or not ill, whether low or high CD 4 counts, whether low or high viral loads that Duesberg is entirely and completely correct.

    All of the rest of the hand-wringing about Gallo and Larry and Fauci and Andrew Sullivan and Avian Flu is secondary and un-important to real people with real health problems.

  8. truthseeker Says:

    McK, thank you for telling us that despite what you wrote, which was entirely in defense of Gallo’s conclusion that HIV was the probsble cause of AIDS, you yourself are still openminded, and do not work in the $150 billion skyscraper of HIV?AIDS activity erected on this site. This does not, however, mean that our assumption that you were in that theoretical camp was wrong. It confirms it. Anyone who cannot see that the skyscraper has no foundation and argues that it has support is a supporter of Gallo and his paradigm, and has the responsibility of justifying that support, which has led to hundreds of thousands of people being administered soem very dangerous drugs.

    To ask that we demonstrate that Duesberg is entirely and completely correct is absurd, since that has already been done in the scientific literature, where journals of the very highest reputation and standards have sent his papers to very hostile peer reviewers anxious to find every fault in them, who then failed to find any uncorrectable error, and thus were unable to object effectively to their being published, After their publication, despite promises from Gallo and others to respond, they were unable to do so, except in other venues which were not subject to peer review.

    Perhaps McK you have thought of some objection which these expert and hostile reviewers were unable to come up with, and you can then write a letter and somehow spike Duesberg’s guns. But short of this, you will have to accept that he has only been rejected with political responses and tactics, which should have no place in science, and which reflect the vast sums and high positions at stake.

    This is what real people with real health problems should worry about – that in this case, a paradigm has been flown like a kite and stayed aloft despite the fact that it is supported by nothing but hot air and very unscientific politics and psychology, including the psychology which turns intelligent people such as McK around so that instead of reading and following the best scientific literature, they imagine that Duesberg is expressing an unconfirmed opinion and ask for proof that he is right.

    Of course, the whole idea of asking the critic of an idea for proof that he is right is absurd especially in this case. His very critique stands as proof that he is right. It is the paradigm that has to “prove that it is right”, and so far it is empty handed in proof – no scientific paper yet – in explanation – no scientific paper yet – and in outcome – no vaccine or cure yet, or any sign of one.

    This blog would prefer not to waste its readers time with extended discussions of whether there is proof that there is not a MacDonald’s open for customers on the far side of the moon. If such a hypothesis is floated, we will demand justification for it, and until that justification in terms of reason and evidence is produced we will not believe it.

    What we will not feel bound to do is justify our incredulity that a 9 kilobase retrovirus which effectively mcannot be transferred in heterosexual sex is responsible for a pandemic of immune disfunction spreading around the world, with risk groups varying by continent, no discernible virus in patients, and for which there was no evidence in the paper with which Gallo started this global meme.

    The first thing any real person with real health problems should do is ask why this paradigm should be believed, not why it should not be believed.

    That is why this blog exists, as noted in our subtitle.

  9. HankBarnes Says:

    McKiernan,

    Hey, it is good to see you digging into the science!

    At this url: http://query.nytimes.com/gst/fullpage.html?sec=health&res=9F0CEFDA103DF932A05751C1A964958260

    Here’s the NY Times, discussing, er, the inconvenient fact, that much of Gallo’s work was fraudulent.

    Care to comment on this, Mack? — Or is this not relevant as you told me before:)

    Your pal,

    Hank B.

  10. McKiernan Says:

    To clarify my position and not have one imposed on me by Truthseeker or others what I am saying is:

    “The simple truth is that HIV cannot simply be jettisonned from the AIDs paradigm as some sort of innocent bystander.”

    The issue isn’t whether I agree or disagree with Dr. Duesberg. The issue isn’t about Gallo. And the issue isn’t whether I live in a $ 150 billion HIV skyscraper.

    If (as others have said) , “the progressive loss of T cells and clinical symptoms of AIDS that follow are still largely restricted to HIV infected individuals” and if it is also true, “as long as viral loads, CD4+ T cell counts and degree of T cell activation correlate with disease progression and as long as treatments that reduce viral loads improve symptoms” then jettisoning HIV isn’t sound science or sound medicine if the clinical facts correlate to the clinical treatment.

    Another commenter here made an important statement on April 11, 2006:

    “Also, it is very important to remember that although Dr. Duesberg’s theory is compelling, his data is all correlational — it doesn’t prove causation. In order to do that, he would have to explain, in terms of our physiology, exactly how it is that exposure to chemicals and toxins depletes the immune system. This is not just a problem in his theory, it is a problem in all theories of AIDS currently. Not one theory, including the HIV theory and the nutritional deficiency theory, has yet to identify the causal mechanism. This is what we must push for. We need to understand exactly how HIV, or chemicals, or nutritional deficiencies end up destroying the cellular immune response. No theory has done that yet. So we are out here on our own without a theory of causal mechanism. Correlations are interesting, and each theory can point to many interesting correlations in support of their theory, but none so far has a clear idea of how T4 Lymphyocytes actually decline — and that is the key to understanding AIDS. I’m insisting, these days, that all of these scientists focus on that question. We all should insist on that.”

  11. Glider Says:

    McKiernan et al,

    I have a question that I’ve long wondered about. Perhaps you can help me. On what basis can the HIV theory of AIDS be falsified? In other words, what data, what evidence, would convince you that the hypothesis is incorrect?

    As I understand it——though I’m neither a scientist nor a philospher——Karl Popper considered falsifiability to be the crucial feature of a sound scientific hypothesis. How then can the reigning view of AIDS be falsified?

    Glider

  12. Mark Biernbaum Says:

    McK — you should at least acknowledge your sources! That’s my statement on causal mechanism — thanks. And Glider — no, it can’t be falsified.
    Mark Biernbaum

  13. McKiernan Says:

    Mark,

    I stand so corrected. Thank you. Yes, it was your statement.

    In the statement above yours, the quoted material was from Dale in a comment on another blog site.

  14. Dale Says:

    Mark,
    Sure the HIV hypothesis can be falsified. Effectively vaccinate to protect against HIV or cure HIV infection and show that it has no effect on the incidence of AIDS related diseases. Alternatively, identify a treatment that improves symptoms (e.g. reverses T cell decline and/or other markers of immune dysfunction) without affecting viral loads. Either of those actions would at least call the HIV hypothesis into serious question.

    Dale

  15. HankBarnes Says:

    Hi Dale,

    Alternatively, identify a treatment that improves symptoms (e.g. reverses T cell decline and/or other markers of immune dysfunction) without affecting viral loads

    This is new!!!

    How about this: Examine other things that may cause T4-cell decline, and ensure that AIDS patients don’t have them.

    A lotta things cause a person to lose T4-cells, right Dale?

    Hank B

  16. Dale Says:

    Yes, Hank, there is more than one factor that can cause T4 cell loss and immunosuppression. Nobody has ever said there wasn’t. The issue is whether HIV is one of them. To falsify that hypothesis, you need to explain all the observations demonstrating that active HIV infection and a propensity to develop progressive immunosuppression are highly correlated in any number of populations. Throw in the animal studies and the laboratory studies that provide at least a partial explaination of how HIV might cause AIDS and it becomes increasingly difficult to see where support for an alternative explaination is going to come from unless it’s from a cure for the immunosuppression that doesn’t affect viral replication.

  17. HankBarnes Says:

    Hey, I like this progress.

    Yes, Hank, there is more than one factor that can cause T4 cell loss and immunosuppression

    So, therefore, it is imperative for HIV+ folks to rule out these “factors” before attributing the depletion in T4-cells to HIV, right?

    Nobody has ever said there wasn’t.

    Awkward construction, double negative, unecessary to central point.

    The issue is whether HIV is one of them.

    Excellent! In full agreement.

    To falsify that hypothesis, you need to explain all the observations demonstrating that active HIV infection and a propensity to develop progressive immunosuppression are highly correlated in any number of populations.

    Close, but muddled. To falsify that hypothesis, you need to show that HIV doesn’t kill T4-cells and/or T4-cells are killed by one of the “factors” described above, rather than HIV.

    Throw in the animal studies ..

    We’ve injected chimpanzees, rats and tons of animals with HIV — none of them develop AIDS, none of them lose T4-Cells.

    …and the laboratory studies that provide at least a partial explaination of how HIV might cause AIDS …

    Partial explanation? Doesn’t HIV infect and lyse the T4-cells .. or is it apoptosis … or is it auto-immune response or is it a mysterious co-factor?

    … and it becomes increasingly difficult to see where support for an alternative explaination is going to come from unless it’s from a cure for the immunosuppression that doesn’t affect viral replication.

    Don’t follow you here. Sounds like you’re prejudging the issue, but Hey, we have progress.

    Hank B

  18. Trevor G Marshall Says:

    I was just conducting a search of literature which linked the secosteroid 1,25-dihydroxyvitamin-D with HIV, and I came across one of my BMJ writings on this site at URL http://www.rethinking.org/bmj/response_55974.html

    An earlier set of my thoughts can be found near the bottom of this letter to the Editor of CHEST http://www.chestjournal.org/cgi/eletters/124/1/6

    Over the last few years I have gradually been developing, and proving, a pathogenesis for chronic immune disease, the subset which is called “Th1,” characterized by excess production of Interferon-gamma, and by the seco-steroid whose production it catalyses, 1,25dihydroxyvitamin-D

    At this point we have developed the science to a state of relative sophistication, having noticed the essential role of the VDR nuclear receptor in Th1 immune disease. We recently published a paper Common angiotensin receptor blockers may directly modulate the immune system via VDR, PPAR and CCR2b.

    We also delivered a “Visiting Professor” presentation to the FDA CDER at which we emphasized how the VDR Nuclear Receptor is at the heart of the homo sapiens’ innate immune response, and examined a number of drugs which affect the operation of the VDR (there is a DVD available from the Foundation, and a low resolution online version this URL

    In June, the non-profit which is the vehicle for the ongoing research of myself, and my colleagues, is to hold a conference in Los Angeles. The keynote speaker is Alan Cantwell, MD. Info is at URL http://www.autoimmunityresearch.org/lax2006.htm

    Now before we go any further, I want to say that my current best guess at tying together Alan’s thoughts, and my own thoughts, is that although HIV is definitely the trigger for the destruction of the immune system which leads to clinical AIDS, I do not believe it is the only factor.

    Indeed, I have shown that Sarcoidosis, an infrequent but definite ‘complication’ in folks recovering from HAART, is solely caused by a heavy load of intraphagocytic bacterial pathogens ( Sarcoidosis succumbs to antibiotics—implications for autoimmune disease)

    There is no doubt whatsoever about the pathogenesis of Sarcoidosis (although it will take TPTB a couple of decades to assimilate what we have done). Intraphagocytic bacteria, chronic pathogens which have evaded phagocytosis, and parasitized the immune system, are the sole cause of this disease. Further, we have shown, to this point anecdotally, that the infection leading to Sarcoidosis develops over a lifetime, and not in the 2-3 months typically seen between when a patient comes off HAART and when they develop Sarcoidosis.

    The inference that I draw from this is that the diseases which follow HIV infection are most probably due to a combination of that HIV infection and a lifelong accumulated load of bacterial pathogens.

    At our Chicago conference last year (in my ‘Can I catch it’ presentation) I described how horizontal-DNA-transfer from a lifetime of viral infections, most probably interspersed with horizontal-DNA-transfer between the chronic bacterial pathogens, determines the course of Th1 disease, and determines which of the ‘autoimmune’ diagnoses a person would progress towards as they age.

    The key to understanding how the bacterial and viral pathogens interact is to note the action of HIV, which has been known for a decade to suppress the production of 1,25dihydroxyvitamin-D in the phagocytes.

    This seco-steroid is the sole known activator of the VDR Nuclear Receptor, and the VDR is at the heart of innate immunity. Without 1,25dihydroxyvitamin-D the innate immune system cannot function. The body is unable to mount a useful response to either the HIV itself, or to the chronic bacterial pathogens.

    The literature search which led me to this site is aimed at determining if any molecular biologists have yet identified the exact pathway for this 1,25dihydroxyvitamin-D suppression, whether it be by inhibition of CYP27A1, CYP27B1, or some other less obvious pathway.

    So I drop my thoughts into the mix. In summary I guess that I am saying that “all of the people might be right some of the time.”

    I personally know that well-hidden, chronic, bacterial pathogens lead to the Th1 immune disease. I suspect they may also be the primary cause of the reduction in the Quality of Life, disease, and death, which result from HIV infection. Disease states which linger, even after HAART has reduced the viral load to minimal levels.

  19. truthseeker Says:

    Hank.for some reason the link you provided above on 4.24.2006 at 3:44pm to the New York Times article, Federal Inquiry Finds Misconduct By a Discoverer of the AIDS Virus, may not show up on some Macs. We have therefore spelled it out in your comment post, as well as retained the link form in case it works on other computers.

    Here is another url and link to a Times review of John Crewdson’s 800 page book, which thoroughly reviewed the father of all HIV?AIDS scientists and his progress through the scientific universe.

    Autopsy of a Medical Breakthrough, by John Horgan, review of

    SCIENCE FICTIONS, A Scientific Mystery, a Massive Coverup, and the Dark Legacy of Robert Gallo. By John Crewdson. Illustrated. 670 pp. Boston: Little, Brown &Company. $27.95.

    In case that doesn’t show in your browser, it reads as a url as this:

    “http://query.nytimes.com/gst/fullpage

    .html?res=9406E2DD123EF930A35750C0A964

    9C8B63&sec=&pagewanted=print”

    “Gallo initially denied that his virus and the French virus were the same. When that position became untenable, he suggested that the French laboratory had misappropriated his virus, not vice versa; after all, he had supplied the French with samples of his virus in the summer of 1984. But Montagnier’s group had described LAV in print a year before they received samples of HTLV-3B from Gallo. Also, Popovic, who had supposedly isolated HTLV-3B, was vague about its origins. Popovic eventually said he had extracted the virus from a ”pool” of blood from many patients, a procedure frowned upon by other virologists.

    “Meanwhile, both the Pasteur Institute and Gallo’s team applied for patents for a test that could detect the virus. After the Patent and Trademark Office awarded the patent to Gallo’s group in May 1985, the Pasteur Institute sued, contending it had discovered the virus used in the Gallo test. When the French produced supporting records, Gallo retorted that their ”meticulous and apparently premeditated documentation” showed they cared more about ”patents and notoriety” than about good science. He also kept churning out revised versions of his own discovery of the AIDS virus, contending in one paper that he had isolated it as early as 1982…”

    “On July 11, 1994, that department finally acknowledged that ”a virus provided by the Institut Pasteur was used by National Institutes of Health scientists who invented the American H.I.V. test kit in 1984.” It promised the French $6 million in restitution. That is as close as the United States has come to an apology for its decade-long defense of Gallo. That year Gallo left the National Institutes of Health for a position at the University of Maryland, but he continued to receive $100,000 annually in royalties for his patented blood test.

    “Gallo and his advocates have portrayed him as a flawed, but great, scientist trying to seek truth and save lives while others tormented him with legalistic quibbles. But the Office of Research Integrity asserted in 1993 that Gallo ”seriously hindered progress in AIDS research” by slighting the French discoveries for so long. His steps to deny the French the United States patent for the blood test, Crewdson suggests, also had dire consequences. Various studies showed that, at least through 1986, Gallo’s test was inferior to the Pasteur version; some Americans were infected with AIDS after receiving blood certified as safe by Gallo’s test. These infections might have been prevented if the French had been granted the United States patent — and the share of the blood-testing market — they deserved. …”

    Horgan’s review, in the newspaper that has always been as soft on Gallo as it has been on his favorite virus, was noticeably missing any words of comfort to the original discoverer of the unexpected possibility of hoodwinking the entire world for twenty years with a paradigm if you cannot play three card monte with a virus and win. In fact, John even suggests that Bob may have been mentally disturbed.

    If so, we challenge anyone to prove he was any more disturbed than the rest of the world who have followed in his footsteps over what the literature suggests is a very high cliff.

  20. truthseeker Says:

    “Now before we go any further, I want to say that my current best guess at tying together Alan’s thoughts, and my own thoughts, is that although HIV is definitely the trigger for the destruction of the immune system which leads to clinical AIDS, I do not believe it is the only factor.”

    Trevor, what a wonderful post. Thank you so much for sharing your ongoing speculations, which may well result in further productive speculations, and so on.

    We were wondering, however, if you would share with us the justification for your use of the word “definitely” in the above excerpt.

    It is interesting that you are now convinced that HIV is not the only factor which causes chronic immune dysfunction. Have you alerted Anthony Fauci at the NIAID of this conclusion? He may find your research enlightening, since he has long seemed to resonate only to the theme initiated by Robert Gallo and David Baltimore that HIV is the only factor worth considering. Indeed, Gallo et al (presumably including Dr Fauci) were notoriously resistant to Luc Montagnier’s arrival at the San Francisco AIDS Conference at the start of the nineties, to announce he had identified the co-factor involved as a mycoplasma he had just discovered.

    Instead of being welcomed, Montagnier found himself having to announce this breakthrough to the world’s press in a cramped hotel facility outside the gates of the Conference site, and when no one among his colleagues would have dinner with him thereafter, having to catch the next plane back to Paris.

    You may have better luck, however. We hope so. We particularly like your remark

    “The inference that I draw from this is that the diseases which follow HIV infection are most probably due to a combination of that HIV infection and a lifelong accumulated load of bacterial pathogens.”

    Could it be that if you added the drugs involved to the mix – you seem to have inadvertently overlooked them as a possible cause of immune problems – we might even have enough impact to just take out the HIV infection altogether?

    That’s why we ask the question at the head of this comment, and look forward to your answer. Whatever it is, we certainly look forward to hearing about your several talks at LAX 2006.

  21. Trevor G Marshall Says:

    Could it be that if you added the drugs involved to the mix?
    Yes, the protease inhibitors are reported to have a direct effect on 1,25-dihydroxyvitamin-D and therefore on the VDR, and therefore on the ability of the immune system to deal with chronic bacterial pathogens. You will find I always disregard the effects of the palliative drugs before I evaluate a disease pathogenesis, and that is why I didn’t mention the drugs.

    The word “definite” should be read as “on the basis of everything I can understand” rather than as an absolute. What I understand is that folk who progress to serious chronic Th1 diseases, like Rheumatoid Arthritis, Sarcoidosis, MS and ALS, seem to steadily accumulate the pathogens during life, and then an opportunistic infection, which may be viral or bacterial, “pushes them over the edge.” I see the same model in HIV infection. That folks collect the ‘predisposing infection’ during gestation and during life. It is just that HIV really does shut down the VDR really ‘well’, and therefore shuts down innate immunity, more effectively than the other viral infections we have come across (the effect of HIV on the VDR is well documented – search PubMed for HIV and dihydroxyvitamin:)

    I sympathize with Montagnier. We ourselves are only just starting to emerge from that phase right now. I personally haven’t worried about Dr Fauci, all my efforts have been directed at Dr Zerhouni himself. Last September a group of recovering Sarcoidosis patients demonstrated during a meeting being held by Dr Zerhouni, so his deniability has disappeared. But there is still a big problem at NIH. There are too many people in positions of authority that have no concept whatsoever of molecular biology, and have evolved a concept of medicine based only on the epidemiological trials referred to as “evidence based medicine.” We all know this paradigm has failed, but it will not disappear until something else arrives to replace it. That is what we are focusing upon. A replacement paradigm. We are making baby-steps – the FDA OPD just designated minocycline in the therapy of Sarcoidosis – and we are currently in vigorous discussion with the FDA Office of the Commissioner, but it is too soon to see how they will react. I would characterize NIH’s current position as “wishing we would go away” – “wishing” because they have been unable to hasten our departure from the scene.

    Alan welcomes the opportunity to share his insight into disease at the June conference, as do I, and there will be plenty of recovering immune patients there who can share their experience of what these pathogens can do to one’s life, in the absence of any HIV infection. I hope that we can generate a vigorous interchange, and finally start to move towards a better understanding of all immune disease, including AIDS.

  22. Robert Houston Says:

    It is apparent that Dr. Trevor Marshall has been conducting important and promising research in regard to sarcoidosis and autoimmune diseases and their relationship to vitamin D physiology. It is to be hoped that the FDA and NIH would cooperate in furthering this scientist’s humane efforts instead of taking their usual obstructionist stance towards independent research.

    Regarding HIV, however, Dr. Marshall has used an unusual and possibly hypothetical rationale to justify a putative pathogenic role. He states above:

    It is just that HIV really does shut down the VDR really ‘well’, and therefore shuts down innate immunity, more effectively than the other viral infections we have come across (the effect of HIV on the VDR is well documented – search PubMed for HIV and dihydroxyvitamin:)

    I have conducted the literature search he recommended and found 28 abstracts, none of which appear to support his assertion of an effect of HIV on the VDR (vitamin D receptor). Possibly he was referring to studies on monocytes in the mid-1990s regarding a difference in effects of vitamin D given at different times, but this is a far cry from the conclusion that HIV “shuts down innate immunity” or the VDR. Those studies drew no such conclusions.

    Could Dr. Marshall please cite which papers he had in mind (or at least one or two) that would indicate that HIV shuts down the VDR? Studies that show a difference in vitamin D utilization in AIDS patients would not constitute such evidence, since these patients have confounding variables of multiple nutritional deficiencies and damage to the liver and immune system from drug abuse and medications.

  23. Trevor G Marshall Says:

    The VDR is uniquely believed to be activated by the seco-steroid 1,25dihydroxyvitamin-D. The levels of this hormone are profoundly affected during HIV infection. Ergo, the function of the VDR is also profoundly affected during HIV infection.

    For more background please take a look at our recent paper:

    Marshall TG, Lee RE, Marshall FE: Common angiotensin receptor blockers may directly modulate the immune system via VDR, PPAR and CCR2b. Theor Biol Med Model. 2006 Jan 10;3(1):1. Available from URL http://www.tbiomed.com/content/3/1/1

    and my recent presentation at the FDA:

    Marshall TG: Molecular genomics offers new insight into the exact mechanism of action of common drugs – ARBs, Statins, and Corticosteroids. FDA CDER Visiting Professor presentation, FDA Biosciences Library, Accession QH447.M27 2006

    Streaming video available from URL http://tinyurl.com/pzw6n

    A PDF of the slides is available from URL http://tinyurl.com/o3du2

    Pasteur said that “in science, chance favors the prepared mind.” I think that what he was trying to say is that if you are waiting for somebody to tell you something in explicit, absolute terms, you will miss the ‘eureka’ moment of discovery. That ‘eureka’ moment comes when you put 2+2 together to make 4, even though 4 is not explicitly called out in what is obviously before you 🙂

    I appreciate your question. If those citations don’t answer the issues, then please do not hesitate to ask again.

  24. Robert Houston Says:

    Dr. Marshall proposed a novel mechanism of HIV pathogenesis that may be news even to NIAID director Fauci, who has admitted to beng puzzled as to how a virus that’s virtually absent can be producing all the mayhem for which it’s been tried and convicted by press conference. It thus seemed appropriate to explore Dr. Marshall’s explanation a bit further.

    I am grateful for the clarification he has provided. Before posting my inquiry, I had already consulted his paper that he cites above; it provides useful information on the VDR (vitamin D receptor) but does not mention HIV. A Medline search for HIV and VDR yields a grand total of two papers: these concern genes for VDR, not an effect of HIV upon it. So what was the basis for his claim that “HIV really does shut down the VDR really ‘well’, and therefore shuts down innate immunity”? Dr. Marshall’s answer is that HIV doesn’t do it directly; rather, the lack of the active vitamin D metabolite in HIV/AIDS patients is the problem. He states:

    The VDR is uniquely believed to be activated by the seco-steroid 1,25dihydroxyvitamin-D. The levels of this hormone are profoundly affected during HIV infection. Ergo, the function of the VDR is also profoundly affected during HIV infection.

    In other publications, Dr. Marshall has noted a similar loss of the vitamin D hormone in advanced cancer. It also declines in kidney malfunction, and other conditions – all without HIV . A common fallacy in AIDS research to attribute any and all concomitant phenomena to the the virus. Meanwhile, the recreational and antiretroviral drugs to which these patients have been subjected routinely cause kidney damage (AZT, for example, is nephrotoxic ), which might also result in impairment of the production of the vitamin D hormone since the kidney is the main site for its production. Apparently there’s no direct evidence that HIV is even involved.

    In my literature search, the earliest report of low levels in AIDS of the active vitamin D metabolite was a 1993 American study which found it deficient in 10% of HIV/AIDS patients (1). Subsequently, researchers at the Univ. of Oslo found low levels in about half of their HIV/AIDS cases (2). They did not, however, attribute this to a direct effect of HIV. They pointed out that “renal dysfunction affecting hydroxylation cannot be excluded,” and that there was an inverse correlation with levels of tumor necrosis factor-alpha (TNF-a), which tends to be high in AIDS patients. They proposed the inadequte hydroxylation of vitamin D was due to an inhibitory effect of elevated TNF-a (2).

    Some of the same Norwegian scientists later reported that TNF-a is elevated in vitamin A deficiency, and can be lowered in half even by modest supplementation of vitamin A (3). It is relevant that AIDS patients tend to be deficient in vitamin A, as do drug abusers in general. Thus, it is an error to blame everything on HIV, when several potential culprits have not been excluded. Furthermore, the rarity of any active HIV virus in AIDS patients makes any biological effect it might have largely irrelevant.

    1. G. O. Coodley et al. Micronutrient concentrations in the HIV wasting syndrome. AIDS 7:1595-1600, 1993.
    2. C. J. Haug et al. Severe deficiency of 1,25-dihydroxyvitamin D3 in HIV infection. J. Clin. Endoc. Metab. 83:3832-8, 1998.
    3. P. Aukrust et al. Eur. J. Clin. Inv. 30:252-259, 2000.

  25. Trevor G Marshall Says:

    Dear Robert Houston,
    It seems you have failed to grasp even the basics of what I have been saying. I didn’t say that the persisting immune illness (called AIDS) was due to any persistence of the HIV virus, I said the exact opposite, that the virus initially reduces the ability of the VDR to function, and then the bacterial pathogens flourish as the cause of continuing disease.

    I am not going to engage in a “discussion” where “proof” is based on citations to other investigator’s work. It is crazy to make decisions in idiopathic disease based on the failed concepts of the last few decades. That is true also for AIDS. Please cite your own personal knowledge, Sir. That we can discuss. The opinions of third parties are of no relevance unless they are prepared to come here and ‘defend’ them in person (I use ‘defend’ in the scientific sense of ‘defense of a thesis’).

    With respect to the irrelevant issues you raise re kidney disease, I would refer you to a chapter we have just written for a book called “Vitamin D: New Research”:
    Waterhouse JC, Marshall TG, Fenter B, Mangin M, Blaney G: High levels of active 1,25-dihydroxyvitamin D despite low levels of the 25-hydroxyvitamin D precursor – Implications of dysregulated vitamin D for disgnosis and treatment of Chronic Disease. In Vitamin D: New Research. Volume 1. Edited by: Stoltz VD. New York: Nova Science Publishers; 2006. ISBN: 1-60021-000-7

    Anybody who is getting hung up on kidney function, and the tired old concepts surrounding the Vitamins D, needs to, at a minimum, read that chapter very thoroughly.

    What our research has achieved is a quantum leap in knowledge, and it cannot be understood, or expanded, by citing failed old studies from years gone by.

    The rebuttal to every one of your points is contained in the writings I have already made in this thread, and the works they cite. I actually find it interesting that skepticism, which this community has reasonably needed to exercise in the past, might ultimately freeze it into inaction at this historic moment, and thus be its undoing 🙂

  26. truthseeker Says:

    What an extraordinary post, Trevor. Are you sure you said what you meant to say?

    First, you asserted that you were convinced that HIV “definitely” was involved in causing immune deficiency, then when we enquired as to why you thought that, you told us that you thought it caused a Vitamin D deficiency, by acting on the Vitamin D receptor (VDR):

    It is just that HIV really does shut down the VDR really ‘well’, and therefore shuts down innate immunity, more effectively than the other viral infections we have come across (the effect of HIV on the VDR is well documented – search PubMed for HIV and dihydroxyvitamin:)

    although you thought that protease inhibitors caused that deficiency too :

    Yes, the protease inhibitors are reported to have a direct effect on 1,25-dihydroxyvitamin-D and therefore on the VDR, and therefore on the ability of the immune system to deal with chronic bacterial pathogens. You will find I always disregard the effects of the palliative drugs before I evaluate a disease pathogenesis, and that is why I didn’t mention the drugs.

    When asked for the references for that claim of VDR inhibition by Robert Houston, you replied with the suggestion he conduct a literature search.

    But he couldn’t find any HIV-VDR link in it:

    I have conducted the literature search he recommended and found 28 abstracts, none of which appear to support his assertion of an effect of HIV on the VDR (vitamin D receptor). Possibly he was referring to studies on monocytes in the mid-1990s regarding a difference in effects of vitamin D given at different times, but this is a far cry from the conclusion that HIV “shuts down innate immunity” or the VDR. Those studies drew no such conclusions.

    and he asked for more references:

    Could Dr. Marshall please cite which papers he had in mind (or at least one or two) that would indicate that HIV shuts down the VDR? Studies that show a difference in vitamin D utilization in AIDS patients would not constitute such evidence, since these patients have confounding variables of multiple nutritional deficiencies and damage to the liver and immune system from drug abuse and medications.

    You then replied with only quoting yourself:

    The VDR is uniquely believed to be activated by the seco-steroid 1,25dihydroxyvitamin-D. The levels of this hormone are profoundly affected during HIV infection. Ergo, the function of the VDR is also profoundly affected during HIV infection.

    For more background please take a look at our recent paper:

    Marshall TG, Lee RE, Marshall FE: Common angiotensin receptor blockers may directly modulate the immune system via VDR, PPAR and CCR2b. Theor Biol Med Model. 2006 Jan 10;3(1):1. Available from URL http://www.tbiomed.com/content/3/1/1

    and my recent presentation at the FDA:

    Marshall TG: Molecular genomics offers new insight into the exact mechanism of action of common drugs – ARBs, Statins, and Corticosteroids. FDA CDER Visiting Professor presentation, FDA Biosciences Library, Accession QH447.M27 2006

    Streaming video available from URL http://tinyurl.com/pzw6n

    A PDF of the slides is available from URL http://tinyurl.com/o3du2

    With respect to the irrelevant issues you raise re kidney disease, I would refer you to a chapter we have just written for a book called “Vitamin D: New Research”:

    Waterhouse JC, Marshall TG, Fenter B, Mangin M, Blaney G: High levels of active 1,25-dihydroxyvitamin D despite low levels of the 25-hydroxyvitamin D precursor – Implications of dysregulated vitamin D for disgnosis and treatment of Chronic Disease. In Vitamin D: New Research. Volume 1. Edited by: Stoltz VD. New York: Nova Science Publishers; 2006. ISBN: 1-60021-000-7

    You then ventured a very peculiar statement which seemed to say that mere facts in hand weren’t going to stop you from imagining possibilities and making breakthroughs in theory. You suggested that Pasteur and other innovators had to forge ideas with leaps of intuition:

    Pasteur said that “in science, chance favors the prepared mind.” I think that what he was trying to say is that if you are waiting for somebody to tell you something in explicit, absolute terms, you will miss the ‘eureka’ moment of discovery. That ‘eureka’ moment comes when you put 2+2 together to make 4, even though 4 is not explicitly called out in what is obviously before you 🙂

    But having made the leap of intuition you have to back it up with evidence, don’t you? You seemed to acknowledge this by saying if the references you provided to your own paper and presentation were not enough, you would be glad to offer more:

    I appreciate your question. If those citations don’t answer the issues, then please do not hesitate to ask again.

    But when Robert Houston pointed out that your paper you cite does not even mention HIV, and that the only two papers on Medline which mention HIV and VDR concern genes for VDR, and don’t mention any effect of HIV on VDR, and said that if your claim that HIV “really does shut down the Vitamin D Receptor really well” is based on the low level of metabolic activation of Vitamin D (to its hormonal form, calcitriol) observed in HIV positive patients, it is not justified:

    I had already consulted his paper that he cites above; it provides useful information on the VDR (vitamin D receptor) but does not mention HIV. A Medline search for HIV and VDR yields a grand total of two papers: these concern genes for VDR, not an effect of HIV upon it. So what was the basis for his claim that “HIV really does shut down the VDR really ‘well’, and therefore shuts down innate immunity”? Dr. Marshall’s answer is that HIV doesn’t do it directly; rather, the lack of the active vitamin D metabolite in HIV/AIDS patients is the problem. He states:

    —The VDR is uniquely believed to be activated by the seco-steroid 1,25dihydroxyvitamin-D. The levels of this hormone are profoundly affected during HIV infection. Ergo, the function of the VDR is also profoundly affected during HIV infection.

    But Houston noted that in other papers to do with cancer you recorded the same loss of the Vitamin D hormone, and it occurs with kidney malfunction and other ailments without HIV, where the kidney problems in AIDS patients are caused by the drugs they are given, both AZT and ARVs. So why should you think that HIV is necessarily involved?

    In other publications, Dr. Marshall has noted a similar loss of the vitamin D hormone in advanced cancer. It also declines in kidney malfunction, and other conditions – all without HIV. A common fallacy in AIDS research to attribute any and all concomitant phenomena to the the virus. Meanwhile, the recreational and antiretroviral drugs to which these patients have been subjected routinely cause kidney damage (AZT, for example, is nephrotoxic ), which might also result in impairment of the production of the vitamin D hormone since the kidney is the main site for its production. Apparently there’s no direct evidence that HIV is even involved.

    Houston pointed out that Oslo researchers thought that the reason for the Vitamin D problem was probably the kidney malfunction and the high level of TNF in AIDS patients , which probably inhibits the metabolic activation of Vitamin D. Later they found that the deficiency in Vitamin A which is typical of drug abusers is the cause of that high TNF presence, and that giving patients a little Vitamin A reduced it.

    He reasonably concluded that you had failed to provide any reason here why you should blame HIV for this Vitamin D deficiency in AIDS patients and the resulting immune problem when there were these other several reasons for it.

    It did look as if you were simply under the influence of the AIDS meme, whereby HIV is blamed for every part of the decline in AIDS patients’ immune system even though the virus itself is virtually absent.

    If the researchers in Norway wrote further papers accounting for the Vitamin D problem you mention by saying that it wasn’t caused by HIV, but was in their analysis caused by kidney problems , and the TNF that accumulates in the wake of a Vitamin A deficiency, why do you then make the extraordinary statement that you don’t want anyone to refer to any more papers, they should speak from their own experience.

    I am not going to engage in a “discussion” where “proof” is based on citations to other investigator’s work. It is crazy to make decisions in idiopathic disease based on the failed concepts of the last few decades. That is true also for AIDS. Please cite your own personal knowledge, Sir. That we can discuss. The opinions of third parties are of no relevance unless they are prepared to come here and ‘defend’ them in person (I use ‘defend’ in the scientific sense of ‘defense of a thesis’).

    In your case you say that your own thinking has been fully explained in your own paper and what you have said here in your posts, and in the chapter of a book that you have written.

    But that is exactly the point. On what papers do you base your own findings that you write about in your book – are they all your own papers recording your own experiments?

    What we are interested in is what reason do you have to suppose that HIV is involved in causing Vitamin D problems, or indeed anything at all? You haven’t yet suggested one here except that HIV is around at the time the problems occur. Aren’t you rather like a policeman who hauls in bystanders who are merely watching a crime but not participating in it?

    We are afraid that you are upset that we have indvertently shot down your pet theory on its way to a triumphant exposition at the upcoming conference, since the belief which doesn’t appear after all to have any justification in the literature. But hopefully this is wrong, and your book or some other source contains the citations needed, If so can you quote a few?

    Alan welcomes the opportunity to share his insight into disease at the June conference, as do I, and there will be plenty of recovering immune patients there who can share their experience of what these pathogens can do to one’s life, in the absence of any HIV infection. I hope that we can generate a vigorous interchange, and finally start to move towards a better understanding of all immune disease, including AIDS.

    The last comment, which you actually made at the start of the exchange, is also mysterious, since you say your interest will be in what the patients have to say about pathogens “in the absence of HIV infection”.

    So apparently HIV is not involved after all? Your final statement is this:

    It seems you have failed to grasp even the basics of what I have been saying. I didn’t say that the persisting immune illness (called AIDS) was due to any persistence of the HIV virus, I said the exact opposite, that the virus initially reduces the ability of the VDR to function, and then the bacterial pathogens flourish as the cause of continuing disease.

    In other words, the basics of what you are saying is that you feel HIV is only involved at the outset in reducing Vitamin D receptor function, and then it is the accumulating pathogens totally wreck the immune system. Fair enough. But surely we may then conclude that if you cannot provide evidence that HIV is involved in the former, then the drugs and the pathogens are the entire problem?

    First the recreational (if not them, then the later palliative) drugs that you don’t mention, then decline of the immune system, then pathogens, OK? No HIV action needed at all.

    You end with this statement:

    I am not going to engage in a “discussion” where “proof” is based on citations to other investigator’s work. It is crazy to make decisions in idiopathic disease based on the failed concepts of the last few decades. That is true also for AIDS.

    Well. The first part seems totally “crazy” to us, and the second part seems totally correct! A statement in science is usually backed up by quoting the peer reviewed paper which justifies the contention. Do you have some other modus operandi to offer?

    But as to the “failed concepts of the last few decades in AIDS”, this seems most enlightened. It seems that your work on VItamin D is interesting in its own right, and we hope you will expound on it further.

    You said re the NIH that

    But there is still a big problem at NIH. There are too many people in positions of authority that have no concept whatsoever of molecular biology, and have evolved a concept of medicine based only on the epidemiological trials referred to as “evidence based medicine.” We all know this paradigm has failed, but it will not disappear until something else arrives to replace it. That is what we are focusing upon. A replacement paradigm. We are making baby-steps – the FDA OPD just designated minocycline in the therapy of Sarcoidosis – and we are currently in vigorous discussion with the FDA Office of the Commissioner, but it is too soon to see how they will react. I would characterize NIH’s current position as “wishing we would go away” – “wishing” because they have been unable to hasten our departure from the scene.

    Does this say what you meant to say? The paradigm of “evidence based medicine” has failed because it is too much based on epidemiology? And you intend to replace it with molecular biology? We hope you will clarify this thought for us, because it is certainly true that HIV?AIDS is based purely on an epidemiology which counts correlation as causation, but without any real evidence for that jump.

    Unfortunately, it appears that you have made the same jump in regard to HIV and Vitamin D. Do you have any citations that back it up?

  27. Robert Houston Says:

    I appreciate Dr. Trevor Marshall’s reply. My remarks were not intended in any way to deprecate the value and importance of his research on metabolic aspects of vitamin D in relation to immune function in various conditions. I was only questioning his specific claim that HIV per se was the cause of the decline in the active metabolite of vitamin D in HIV/AIDS patients. Since I quoted him directly and at length, it does not appear that there was any misrepresentation of his view. He put it quite directly in his first comment, “HIV is definitely the trigger for the destruction of the immune system which leads to clinical AIDS.”

    This statement has no evidential basis. In subsequent comments, he made similarly groundless claims that “HIV really does shut down the VDR” (vitamin D receptor) “and therefore shuts down innate immunity.” When I innocently asked for a reference or two, he cited only a paper by himself that does not even mention HIV or AIDS.

    Apparently, his new rules for discussion are that no publications are to be mentioned except his own. (This seems like a strange rule for a scientist, but hey, we all have our foibles.) He even expressed annoyance that I cited actual studies. Two of my three citations were to later publications by the same Norwegian research team that he cited in his 2004 BMJ communication and whose findings seem to be the main basis for his claims. They presented plausible non-HIV explanations for the lowered levels of the active vitamin D metabolite in AIDS patients, namely an inhibitory effect of elevated TNF in AIDS, more rapid turnover of immune cells, and possible kidney dysfunction.

    Dr. Marshall seems particularly annoyed that I should mention the kidney – does he deny that it’s the main site for the production of the vitamin D hormone (1,25-dihydroxyvitamin-D3, or calcitriol)? In addition to kidney disease, a number of other non-HIV conditions are associated with low levels of the D-hormone, including cancer, diabetes, tuberculosis, septicemia, myelomatosis, etc. Furthermore, a number of drugs have been shown to lower its levels, including antiretrovirals (e.g. protease inhibitors), corticosteroids, the antifungal agent ketoconizole, and even alcohol — all of which are widely used by people with AIDS. (For technical readers who do want a reference: these facts are documented in Chap. 74 of the of the textbook Vitamin D , Ed.: D. Feldman et al., 2005.)

    The meaning of this information is that HIV is completely unnecessory to the decline of calcitriol – in AIDS or any condition. Furthermore, there is no evidence that I can find or that Dr. Marshall has provided that HIV has any direct effect in lowering calcitriol. Moreover, even if it had such an effect en masse, this would be irrelevant to the actual clinical situation of AIDS, for active HIV occurs in less than one in six million immune cells, as I documented in a previous COMMENT.

    I look forward to reading Dr. Marshall’s new chapter on vitamin D when the volume in which it appears becomes available.

  28. Trevor G Marshall Says:

    Dear Dr Houston,
    I am glad you have all the answers. When you can sit down with me and discuss the depth of molecular science which is in my recent paper(s) on the VDR, then we can start to move forward, but right now I will leave you floundering in the failed and incorrect concepts of the pre-genomic era.

    Sincerely
    Trevor

  29. truthseeker Says:

    Trevor, you now place the host of this site in a difficult position, that of having to write up this exchange in a full dress post on the blog as a prime example of the action of the AIDS meme, which once having invaded the brain of the scientist thereafter rules even at the cost of reason and evidence, and in fact resists surgery to the extent of grabbing the surgeon’s tools and throwing them out of the window.

    The difficulty is that we do not wish to detract from the stature and reputation of any of our guests.

    In the first place, why the putdown of the esteemed nutritional authority Robert Houston, who merely asked for references for your statements, and offered the same for his own, thus maintaining standards at this site which after all exists to apply the lens of the literature to the fantasies and fictions of the HIV?AIDS arena?

    It seems that Robert Houston has you at a disadvantage because he can easily cite references and you cannot. Even though you offered citations, you become brusque and dismissive when they are requested. Now you abandon ship and flee inland with the Parthian shot that anyone who challenges your HIV-VDR claim will find the answer in “the depth of molecular science” in your own papers.

    Surely providing references is merely a matter of going to your computer or library and firing up PubMed, which is accessible to all. Are you not aware of its advantages? There are about 16 million papers on it and counting, including your own.

    If there are no references on PubMed backing your contention that HIV is in some way responsible for deactivating the Vitamin D hormone receptor, why not abandon it? Surely you do not feel yourself shackled to the party line in AIDS, which is that HIV is responsible for every ailment in the field other than the habit of writing spurious papers for publication in Science.

    Or is it that you reasonably feel that subscribing to the notion that HIV has to be involved in all matters to do with HIV?AIDS is a sine qua non of obtaining funding of the kind you are now seeking? If that is true, we certainly understand.

    As to floundering in the concepts of the pre-genomic era, this remark confirms that you have joined the vast crowd of scientists who ever since Jim Watson and Crick solved the structure of DNA have focused on the gene as holding the secrets of the medical universe. But isn’t the lesson of the last few decades the dangerous sterility of that focus? Why do you think that oncogenes have proved such a cul-de-sac in cancer research? Surely it is the environment as well as the gene which is important, and we have learned just how complex the interaction is.

    Perhaps we should be living in the post-genomic era. But either way, it is hard to see why HIV “definitely” is “the trigger for the destruction of the immune system which leads to clinical AIDS”. And your last response to the request for references is a little abrupt.

    To the onlooker, unfortunately, it appears that you are the one who is floundering, since you cannot back up what you are saying with anything better than hints that your papers explain all. Since they don’t appear to mention HIV in any signifcant manner, how does this work?

  30. Trevor G Marshall Says:

    Dear Truthseeker,
    Let’s leave it that way then. You are convinced that I am the one who does not have his ducks in a row, so let’s let History be the arbiter of that. I really am very busy right now, preparing for two conferences within the next month. Yes, I can pull citations from PubMed, but so can you. I will move on and leave you alone again, content with the certainty that PubMed can supply the answers this community needs.

    I have never suffered from HIV or AIDS, I have no friends with HIV or AIDS, I was here purely trying to help. Everything I posted was factually accurate exactly as written. Again, history is an impartial arbiter. I have time to await the judgement of history.

    Sincerely
    Trevor

  31. truthseeker Says:

    So you have retired, injured, Trevor? OK, let’s review your performance.

    You have expressed your conviction that HIV is responsible for immune dysfunction, “definitely”, and when asked how, told us that it triggers Vitamin D hormonal deficiency by interfering with the Vitamin D hormone receptor. When asked for any references at all to back this contention, you tell us to read your papers, and when we do and find no relevant explanation or even significant mention of HIV, and that the only citation you can offer was changed by the authors themselves in later papers, you promise further citations, and then renege when they are requested, and when confronted with references showing that what you believe is better explained without any action by HIV in ordinary scientific terms, grow agitated, object to any references at all except your own writings, and state in bold font Please cite your own personal knowledge, Sir., and now you resign from the exchange, saying History will be the judge, and that you are too busy preparing for two conferences to pull references from PubMed when we can do it ourselves, and that you are not an AIDS patient and know no AIDS patient among your friends, and that you were here only trying to help.

    In other words, you were here trying to help by passing on your novel theory of how HIV works, to people you supposed were HIV?AIDS patients or knew HIV?AIDS patients, and soon you will appear at two conferences with the same mission, where you presumably also expect acclaim and gratitude for yourself and your institution for passing on what appears to be a speculation on your part that has no grounding in fact or literature except your own writings, with a mechanism which you decline to make more specific other than to say that History will be your judge.

    Why is this different from anything else that has been said to date about HIV and how it somehow causes immune dysfunction? Is there any claim for HIV which is not a speculation which entirely lacks proof of any kind and which on the other hand has abundant evidence that the real cause is something else – nitrites causing KS, for example?

    Isn’t the trend of history so far in exactly the opposite direction from that which you hope, that is, always knocking down the claims of HIV?AIDS – that HIV is infectious, for example, or that it kills T cells? Why should it treat your speculation any differently?

    And if your speculation is wrong, why should History be the judge when in the meantime many may suffer from gullibly taking your opinion as gospel, just as hundreds of thousands have suffered by taking the edicts of HIV?AIDS experts as a doctrine by which they must live and die. Don’t we need quicker dispensation than the judgement of history?

    We remain interested in your other speculations regarding Vitamin D if you can back them up any better, but must insist that if you do not have any better reason to imagine HIV causes a problem with Vitamin D hormone than your own desire to fit in with Fauci and Zerhouni for funding purposes, and to advance the cause of your autoimmunity foundation, you should admit it before you exit.

    That is, if you truly want to be helpful to any HIV?AIDS patients who read this, which is an admirable sentiment but surely not realized when you justify HIV as a threat in a novel way which has no basis in the literature, however “definitely” you believe it.

    Otherwise we will have to put you down as yet another confidence man of medicine, who plays with the destinies of the uninformed and trusting by talking hot air until, like snake oil salesmen of old, they are detected as charlatans and hastily fold up their stands and drive their wagons as fast as they can to the next village, where they are once again trusted as authorities out of the ignorance of the vulnerable.

    Tell us this is not true, Trevor.

  32. Robert Houston Says:

    Actually, I don’t think that’s true, Truthseeker. The comparison with “snake oil salesman” and “charlatans” is a colorful but unfair technique often used against those who pursue new directions in natural and biological modalities. Dr. Marshall may indeed have made historically notable contributions toward the resolution of sarcoidosis and autoimmune diseases, while helping to establish better understanding of the manifold implications of vitamin D metabolites for the proper functioning of the immune system. I took issue only with his statements about HIV causation, which as you noted, are really an obligatory form of loyalty oath required of scientists in the field as a precondition for grants.

    If Fauci and Zerhouni of NIAID would contribute a $100 million grant to his Autoimmunity Research Foundation, I have no doubt the results would far exceed the bag of beans we’ve got for all the $140 billions they’ve squandered on the “failed concepts” of HIV/AIDS and other immune disorders.

    If NIAID isn’t interested in vitamin D research, the NCI certainly seems to be. An editorial in the April 5, 2006 issue of their Journal hails new studies indicating marked reductions in cancer mortality from increased levels of vitamin D (click HERE to see it).

  33. Truthseeker Says:

    Well, we certainly didn’t mean to devalue Dr. Marshall’s serious research into Vitamin D phenomena involved in the sickness of HIV?AIDS patients or any others. We said as much – we welcome any more information he cares to impart on the topic.

    This is a site focused very specifically on the relation of the literature in HIV?AIDS to the paradigm, and on the issue of whether that literature supports the paradigm or contradicts it. It appears to do the latter in every respect, and so we are naturally disappointed that Trevor Marshall came up with a possible exception, but proved Alas not to have data to back up his contention.

    We were merely complaining very specifically about his unwillingness to acknowledge that the connection with HIV did not have any backing in the literature, and that he hadn’t discovered anything yet in his own writings which he could offer us, even though he promised to give us more citations if we needed them. We hoped that he would acknowledge this frankly instead of feeling that it devalued his research in any way, because we don’t think it does.

    Instead, he seems to prefer to decamp, which is the only comparison with snake oil salesmen we saw. Unlike such people, he is a serious researcher with interesting findings, and an original mind.

    We also acknowledged that this may only have been a problem because his statement reflected his need to stay on the right side of the NIAID in asking for funding, and we support such a position as entirely practical.

    As to his interest in nutritional aspects of immune dysfunction, we heartily support his efforts and hope that he continues to gain fruitful findings in this area, and will share any he has achieved to date, since this appears to us to be a key to HIV?AIDS which is still overlooked.

  34. Gene Semon Says:

    Gallo does indeed falsify himself as confirmed in:

    Shaw, Hahn, Arya, Groopman, Gallo, Wong-Staal; Science, V226, 1165-1171, 12/7/84

    “HTLV-III (pro)viral DNA can be detected in low levels in fresh (primary) lymhoid tissue of a minority of patients with AIDS or ARC but appears not to be present in Kaposi’s Sarcoma tissue.” (from Abstract)

    “We have described here the molecular cloning and analysis of the full-length HTLV-III proviral genome from the cell line H9/HTLV-III.”

    “In most of the patients in which HTLV-III DNA sequences were detected in fresh tissue, the signal intensities were weak”.

    “In all, HTLV-III sequences were detected in only 9 out of 65 (AIDS) patients evaluated (Table 1). . . None of the five Kaposi’s sarcoma tissue specimens was positive for HTLV-III DNA sequences.”

    Table 1 shows for “clinical diagnosis” of “AIDS (tissue) : 15 (peripheral blood mononuclear cells) samples tested, 1 positive; 19 (lymph node cells) samples tested, 4 positive; 8 (bone marrow mononuclear cells) samples tested, 0 positive; 11 (spleen) samples tested, 2 positive; 5 (Kaposi’s sarcoma) samples tested, 0 positive.” (Note: KS was original “signal” disease)

    “ . . . (A)s shown herein, HTLV-III DNA is usually not detected by standard Southern hybridization of these same tissues (from most patients with AIDS or ARC) and, when it is, the bands are often faint. . . (T)hus, the lymph node enlargement commonly found in ARC or AIDS patients cannot be due directly to the proliferation of HTLV-III infected cells.”

  35. Gene Semon Says:

    It is interesting to note that the esteemed Dr Marshall is actually revealing (5/8/06 post) for our benefit the standard of scientific evidence required in a court of law, which disallows just any scientific paper one cares to introduce in the name of “fairness”.

    A paper must be represented by the author testifying as an expert witness, as if this is the only way this evidence can be “cross-examined”. His (put-down) recitation of this standard, by rote as it were, in the response to Robert Houston only indicates a poverty of the imagination in him and our judicial system.

  36. The Editor Says:

    >>And perhaps your readers will also be appreciate a 1989 report in the Journal of Clinical Microbiology in which:

    >>Human Immunodeficiency Virus type 1 was Detected in All Seropositive Symptomatic and Asymptomatic Individuals and in None of 131 healthy HIV-1 antibody negative individuals.
    What the hell is that supposed to mean? If seropositive for HIV, of course HIV will be “detected” and if HIV-antibody negative, it won’t be.

    Am I missing something ? It’s like saying, “Among 30 Americans who are lactose intolerant, 30 were lactose intolerant.”

  37. Truthseeker Says:

    Good one, Ed. (though sorry, we do not approve of your moniker, which is misleading. If you could see your way to posting under a different tag, it would be appreciated.) Perhaps the intent was to distinguish betwen the presence of actual virus, as determined in the way which has been fiercely questioned later, and the indication of antibodies to it.

    The truth of the matter seems to be that there is so much that is not nailed down in this area, and so many false claims made by Gallo for his lab work which was motivated at the time by the desire to replace the priority of Montagnier with his own claim, falsity revealed in later investigations by NIH officials and others, that you have to be an expert to know what can be taken seriously, if anything at all, in readings of actual viral presence, which is typically verging on non existent once the initial invasive period is over. One dreads to think what an impartial university level enquiry would come up with if it was given the responsibility of checking the lab side of HIV∫AIDS for science, sense and substance.

  38. Truthseeker Says:

    Special note: On the subject of accuracy of tests, and their import, if any, a very important post by Rebecca Culshaw has appeared today on Barnesworld, now renamed “You Bet Your Life”, at Dear Dr. Culshaw: “Well, What About Those Tests?”.

    Culshaw has discovered that the inserts with AIDS tests show that the companies that make them have been backing down over the past year or two in the firmness of their statements that HIV is the cause of AIDS.

    But I doubt even more that the majority of medical practitioners are aware of the subtle but significant shift in the language used in HIV test kits since the beginning of the AIDS era. For example, from 1984 until the very recent past, test kit inserts contained the unambiguous statement “AIDS is caused by HIV”. In 2002, the OraSure toned down that statement to say: “AIDS, AIDS-related complex and pre-AIDS are thought to be caused by HIV.” (Italics mine)

    But just this year, in a remarkable – and potentially significant – shift in thinking, the trend seems to be toward making an even less committal statement. For example, Abbott Diagnostic’s ELISA test insert contains the following sentence: “Epidemiologic data suggest that the Acquired Immune Deficiency Syndrome (AIDS) is caused by at least two types of human immunodeficiency viruses, collectively known as HIV.”

    Vironostika appears to be even less willing to support a true causal role, as their 2006 test kit insert says: “Published data indicate a strong correlation between the acquired immune deficiency syndrome (AIDS) and a retrovirus referred to as Human Immunodeficiency Virus (HIV).”

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