HIV/AIDS Skepticism

Pointing to evidence that HIV is not the necessary and sufficient cause of AIDS

Posts Tagged ‘AIDS as immune activation’

HAART and HIV/AIDS: Dilemmas, Paradoxes, and Errors

Posted by Henry Bauer on 2008/10/12

“The Sink and the Murder Scene: Rise and Fall of a Causal Model for AIDS Pathogenesis” by Vincenzo Crupi (Logic and Philosophy of Science V [#1, 2007] 9-32)  is a clear, concise, fully documented summary of what’s missing in our understanding of several aspects of “HIV” and of “AIDS”; and it illustrates, in my opinion, what’s very wrong with “HIV = AIDS” and “highly active antiretroviral treatment”.

From the very beginning, the central problem has been to understand how “HIV” kills the immune system. That it does so was assumed because of a correlation between CD4+ counts and disease progression (a correlation that has turned out to be anything but consistent) and an apparent preferential association of HIV with CD4+ cells. But — as Duesberg, for one, pointed out early on — a negligible proportion of CD4+ cells in AIDS patients is actually “HIV-infected”. Even in lymph tissue, which was suggested to be a “reservoir”, only about 1% of cells are “HIV-infected”.

To resolve this decade-long dilemma, Ho and Shaw invented a model in which the very low steady-state or average “infection” rate masked an enormously high rate of cell death and replenishment whereupon, after the average “latent” period of about 10 years, the immune-system was exhausted and could no longer replenish. Crupi shows, with citation as well as explication of sources, that this model is disproved by published observations and experiments. Among the salient points is that CD4+ counts in the blood can be misleading because these cells are redistributed as needed throughout various parts of the body (as mentioned previously on this blog in relation to Juliane Sacher’s work — “AIDS as Intestinal Dysbiosis”, 23 February 2008; “Alternative Treatments for AIDS”, 25 February 2008. Moreover, antiretroviral drugs may quickly reduce “viral load” without increasing the life-span of the cells supposedly killed by the virus, indicating that “HIV” is not the agent of cell death.

Because of these findings, mainstream speculation turns increasingly to the view that AIDS is characterized by “abnormal, chronic and up-regulated levels of immune system activation”, which may also occur in absence of HIV. Furthermore, clinical improvement can occur in AIDS patients on antiretroviral therapy even when “HIV” seems little affected. Crupi concludes that research is urgently needed on some of the matters that mainstream HIV/AIDS researchers have largely by-passed.

I strongly recommend this article. The facts about “HIV/AIDS” are at least equally well explained by regarding “HIV” as a sign of immune activation — or physiological stress, or specifically oxidative stress as the Perth Group has it — as by the apparently current mainstream view that “HIV” causes the immune activation that indirectly and eventually depletes the immune system.

I think it’s worth noting that HAART, “highly active antiretroviral treatment”, was designed on the basis of the Ho-Shaw model, which has been thoroughly disproved. It does not necessarily follow that HAART is ineffective, of course — it might by chance have some benefits, it would not be the first medical treatment to work despite misunderstanding or lack of understanding of why it works. As it turns out, though, death statistics  show that HAART doesn’t prolong lives to any significant extent. The discussion and citations in Crupi’s article serve to explain why that’s the case.

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