I find your beliefs very coherent concerning questioning the internal coherence of “AIDS”, but I frankly don’t really care who labels whomever a “dissident” or a “denialist.” I don’t require a label, exactly because I use my real name. I am simply myself.

As for my warm regard for Truthseeker, friendships go through both good and bad phases and both parties make good and bad decisions — you know nothing of my relationship with Truthseeker. I do happen to admire him and am grateful for his dedication, and sometimes he frustrates me. Not abnormal in a friendship, I should think.

I wonder why it is you feel it so necessary to attack me. I certainly am not your enemy in any way. But this kind of talk is clogging what was otherwise a productive discussion on this blog. If you want to continue in your crusade against me, please feel free to do so, but email me directly rather than taking up space here. And if you do me the honor of sending me an email, please do let me know who you really are.

Sorry if you don’t like my handle, but there is no more reason for me to use my name on this blog than there is for “Truthseeker” to use his. Unlike you I believe in working quietly and calmly, and have no desire to be a star gay “positive” dissident. Also unlike you I don’t think CD$ depletion has much to do with what gets called “AIDS.” In fact I am convinced the syndrome itself is incoherent and only leads us away from finding treatments for actual illnesses. I am happy for you that you are so satisfied with your so-called scientific conservatism, although in my view it is the acceptance of the existence of “AIDS” which is dogma. I am surprised to hear you so boldly praise “Truthseeker” when it was not so long ago you were attacking him and trying to lead a campaign to “out” him. I do hope further reading of the history and science will lead you to change your mind about who is and is not a dissident. I hardly see the point of claiming as dissidents people who attack us as :denialists. I will end my part of our exchange here and promise not to respond to you in the future as there really is no point in this exchange.

To Richard: My comments specifically addressed Ho’s model and HAART, which was the most important justification (Times’ Man of the Year, remember!?) for the cocktails you love so dearly. Now you have a new, brand new guaranteed correct theory. And you’re resorting to ad hominem because obviously I am not part of the revised standard official version of your vanguardist movement. You’ve taken a page from the playbook of Vladimir Illich. Congratulations Richard. You’re sure to make Cardinal.

In the meantime. I will continue to make posts that are OF A PIECE and consistent with previous posts and, hopefully, move the discussion forward. If you choose to make progress measured in inches and want to belabor points endlessly, beating your chest to impress all of us with your great knowledge of T-cell dynamics, fine.

Carl T. Bergstrom and Rustom Antia. How do adaptive immune systems control pathogens while avoiding autoimmunity? Trends in Ecology &Evolution . Volume 21, Issue 1 , January 2006, Pages 22-28

EXCERPTS

(B)ecause pathogens interfere with immune function, immune systems must be robust against sabotage. We describe here how these challenges are met by two immune systems, the intracellular RNA interference system and the vertebrate CD8 T-cell response. We extrapolate from these two systems to propose principles for strategically robust control.

By deploying multiple redundant defense pathways, the host can influence the evolutionary trajectory of a pathogen population. Redundant defense mechanisms reduce the selective advantage to the pathogen of knocking out a single mechanism.

Systems that have to deal with internal subversion (and the retrovirus must be demonstrated to reach that stage)* must go one step further and be strategically robust: that is, they need to function properly despite efforts to sabotage their workings. *(added to text)

The distinction between robustness and strategic robustness becomes clear through analogy. A robust computer circuit would function effectively even if a few resistors burned out at random. A strategically robust computer circuit would function even if a disgruntled technician tried to sabotage the machine by removing precisely those resistors that were most crucial. (Added to text: if the AIDS virus can be demonstrated to be equivalent to the “disgruntled technician”, without invoking teleology, then we have something like compelling evidence.)

RNAi is a system of post-transcriptional gene silencing that is broadly conserved across eukaryotes; it appears to have evolved as a form of adaptive immunity to prevent viruses from replicating within infected cells, by targeting foreign nucleic acids. (Added to text: something the classical virologists knew nothing about. Score one for the antidenialists.)

END EXCERPTS

Assuming an HIV “hijacks”, what about the armed guards RNAi?

This paper can be accessed at:

http://www.barnesworld.blogs.com/ => Science Stuff => Trends in Ecology &Evolution

(Posted on 6/22/06)

Response to Richard 6/24, 4:26PM

There is a distinction between “arguing” and defining. I originally stated the possibility of CD3- cells and you replied that CD3 is part of the T cell receptor (not mentioning alpha/beta), by definition on each and every T-cell. I find examples of CD3- cells in ONE NEJM paper at hand and you hand wave about “abnormal”.

My earlier post said “by deploying multiple redundant defense pathways, the host can influence the evolutionary trajectory of a pathogen population. Redundant defense mechanisms reduce the selective advantage to the pathogen of knocking out a single mechanism.”(authors) This was, for your consideration, a network model discussing adaptive responses and functional redundancies of T cells. “Three patients” with “abnormal CD3+CD4-CD8- cells” are suggestive of functional redundancy for the helper/memory function. I make an analogy to an emergency cooling system for a chemical plant reactor, not normally turned on. So nothing here is inconsistent with the idea that detailed understandings of lymphocyte dynamics have different schools of interpretation, which should be a given when evaluating such papers as Hellerstein.

The leukemic effect? You’re really exercised over this one. I would say it’s an effect consistent with severe, life threatening hypersensitivity reactions of HAART NNRTIs. Other effects consistent: eosinophilia(!), lymphadenopathy, general malaise, flu-like symptoms, etc. And let’s not forget that “(mechanism and long term consequences of) redistribution/accumulation of body fat including central obesity, dorsocervical fat enlargement (buffalo hump), peripheral wasting, facial wasting, breast enlargement (are currently unknown)” (PDR, 2006)

(Posted at 4;01PM, 6/27/06)