HIV/AIDS Skepticism

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

Posts Tagged ‘HIV pathogenesis’

HOW does HIV kill the immune system?

Posted by Henry Bauer on 2013/12/24

An alien from another planet, or a naïve believer in the objective nature of science, might imagine that the central, single most important issue of HIV/AIDS theory is the mechanism by which HIV does what it is supposed to do, namely, destroy the CD4 T-cells whose subsequent absence leaves the unfortunate host helpless against opportunistic infections like Pneumocystis carinii pneumonia or candidiasis.

“We probably know more about how HIV produces its pathology than about the pathological mechanism of virtually any other microbe”, Robert Gallo asserted already in 1991 (p. 296 in Virus Hunting: AIDS, Cancer, and the Human Retrovirus: A Story of Scientific Discovery).
That alien and that naïve observer would naturally conclude that by 1991 it was fully understood, how HIV kills T-cells. As a stark matter of fact, though, two decades after Gallo’s assertion, it remains an unsolved enigma, how HIV could possibly do what HIV/AIDS theory demands of it.

Duesberg [1] first posed the conundrum of how HIV could damage the immune system when it is present in only 0.1-1 % of the lymphocytes it supposedly kills, and is expressed in only 1% of those in which it is present. There have been many imaginative speculations about how the tiny minority of infected cells could somehow cause the whole immune system to collapse [2], but those have been countered by Duesberg [3], and in any case none of the suggested mechanisms has been established by actual evidence. A continually updated website [4] mentions a number of possibilities, again none of which has been definitively established.
The current consensus, such as it is, seems to be that cells are killed by an unspecified “bystander” mechanism under conditions of “chronic inflammation” or “chronic activation”. In absence of any specific description of actual processes, those phrases deserve to be described and dismissed as “hand-waving”, the scientific euphemism for bullshit [5], utterances made without regard for their possible truth value. Insofar as chronic activation or inflammation might be interpreted as a high rate of turnover of immune-system cells, it should be recalled that this notion — the basis for introducing combination antiretroviral therapy, Highly Active Anti-Retroviral Treatment, in the mid-1990s — was shown to be faulty [6].

In any case, as of December 2013, after three decades of belief that HIV kills the immune system, there is no agreement over how it could possibly do so. Thus “Despite more than three decades of study, the precise mechanism(s) underlying the demise of CD4 T cells during HIV infection remains poorly understood and has been highlighted as one of the key questions in HIV research” [7].
Note that the common scientific euphemism “poorly understood” stands for “completely unknown”.

Such a stunning admission of the failure of HIV/AIDS theory is, of course, made only in the context of putting forward a new proposed mechanism, in this case “pyroptosis triggered by abortive viral infection”, which also raises “the possibility of a new class of ‘anti-AIDS’ therapeutics targeting the host rather than the virus” [8].

This latest breakthrough was significant enough to be broadcast to the media even before the actual publications had appeared. [8] was even marked “NOT FINAL PROOF”. Observers of the cutthroat competitiveness in research will also note the skill with which much the same work has been published simultaneously in Nature and in Science, and how the media fell right in by parroting the extravagant claim: “How HIV destroys immune cells” [9] — forgetting, apparently, that half a year earlier an entirely different mechanism and potential treatment had been ballyhooed: “Scientists discover how HIV kills immune cells; findings have implications for HIV treatment” [10].

Fauci pronounced the pyroptosis stuff “really elegant science . . . . It goes a long way to explaining what has been an enigma for practically 30 years” — acknowledging once again that the mainstream hasn’t had a clue for 30 years about the central issue in HIV/AIDS theory; and “going a long way” remains far from actually reaching a goal.

Not that this new understanding, with its implication of an entirely new approach to treatment, would actually supersede anything: “Fauci said such an approach would not replace antiretrovirals (ARVs), which suppress HIV replication and halt disease progression. But it could be used in combination in people who are dealing with highly resistant HIV strains . . . . One of the things about blocking the host response is that it’s very difficult for the virus to mutate to counteract it” [9a].

The lead investigator on the pyroptosis work was suitably modest even as he raised highly unlikely possibilities: “If we get rid of chronic inflammation, will we stop the homeostatic proliferation and degrade the latent reservoir? . . . If it does, caspase-1 inhibitors might — and I emphasize might — become a component of a curative cocktail”.

No matter, really. Ample grounds here for lots more research and the associated research funds.

I venture a prediction: None of these hopes and possibilities will pan out, and nothing more will be heard about them in the future.


[1] Peter H. Duesberg, “Retroviruses as carcinogens and pathogens: Expectations and reality”, Cancer Research, 47 (1987)1199-1220
[2]Anthony A. Fauci, “The Human Immunodeficiency Virus: Infectivity and mechanisms of pathogenesis”, Science, 239 (1988) 617-22; Alfred S. Evans, “Does HIV cause AIDS? An historical perspective”, Journal of Acquired Immune Deficiency Syndromes, 2 (1989) 107-13
[3] Duesberg, “Does HIV cause AIDS?”, Journal of Acquired Immune Deficiency Syndromes, 2 (1989) 514-7
[5] Harry G. Frankfurt, On Bullshit, Princeton University Press, 2005
[6] Craddock, “HIV: Science by press conference”, pp. 127-30 in AIDS: Virus or Drug-Induced?, Kluwer, 1996; Duesberg & Bialy, “Duesberg and the right of reply according to Maddox-Nature”, pp. 241-70 in AIDS: Virus or Drug-Induced?, Kluwer, 1996; Roederer, “Getting to the HAART of T cell dynamics”, Nature Medicine, 4 (1998) 145-6; Yates et al., “Understanding the slow depletion of memory CD4+ T cells in HIV infection”, PLoS Medicine, 4 (2007) e177
[7] Monroe et al., “IFI16 DNA sensor is required for death of lymphoid CD4 T cells abortively infected with HIV”, Sciencexpress, / 19 December 2013 / Page 1/ 10.1126/science.1243640
[8] Doitsh et al., “Cell death by pyroptosis drives CD4 T-cell depletion in HIV-1 infection”, Nature, 2013, doi:10.1038/nature12940
[9] 19 December 2013: [a] Dan Cossins, The Scientist;;
[b] Anna Azvolinsky, “HIV’s killer tactics revealed, new therapy approach found”,;
and more
[10] 5 June 2013,

Posted in Alternative AIDS treatments, antiretroviral drugs, experts, HIV absurdities, HIV does not cause AIDS, HIV skepticism, uncritical media | Tagged: , , | 30 Comments »

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.

Posted in antiretroviral drugs, HIV as stress, HIV skepticism | Tagged: , , , , | Leave a Comment »

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