HIV/AIDS Skepticism

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

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,

30 Responses to “HOW does HIV kill the immune system?”

  1. said

    May the truth be recognized and understood, for it has long been known.

    So it goes…

  2. David Crowe said

    If you don’t know HOW you don’t know IF (HIV kills CD4 cells).

  3. Marshall Sandefur said

    They make it like its so complicated. Simply put I have had plenty of sex with women who are HIV positive and none of us are sick and never will get sick. The tests for HIV don’t test for it and the drugs used to treat you are killing you. If we could take the money away from the “epidemic” that would be the end of it. But its a multi-billion dollar industry. All research starts with the belief that HIV causes AIDS. Then they proceed from there, a flawed hypothesis.
    Peace and Blessings,
    Marshall Sandefur

  4. Carol said

    > One of the things about blocking the host response is that it’s very difficult for the virus to mutate to counteract it” [9a].

    I just love it when people who should know better say things like this, things that imply that a virus mutates consciously and with intent.

    • Henry Bauer said

      The genome of HIV may only be 10k in size, but it has outwitted HIV/AIDS researchers for 30 years. Could that mean it’s smarter than they are?

  5. lukas said

    Just yesterday i read about of a new mechanism with which mainstream try to explain cd4 cells depletion.For the first time they recognize what Duisberg had said 30 years ago,that hiv infects very few cells to justify a massive depletion.It seems it took 30 years to state they were looking in the wrong direction.According to the news the last mechanism is called pyroptotis,a self inducted process of distruction that the immunesystem triggers against itself:
    Everytime i read of new mechanisms and super powers of hiv i ask myself if this people is trying to fool humanity much more than how much is able the “alleged” hiv to fool immunity.

    • Henry Bauer said

      I refer to the pyroptosis suggestion in my post, references by Monroe et al. and Doitsh et al.

  6. Liu said

    How about other viral infections ? What’s the percentage of cells it infects to cause illness in host ? I mean Hep B virus doesn’t infect every liver cell for it to cause liver cancer. Or you don’t think there’s a link between Hep B and liver disease neither ?

    • Henry Bauer said

      Hep B, like other viruses that cause harm to human beings, is a DNA virus which replicates directly and destroys cells while releasing many new copies of itself. HIV, however, is a retrovirus, whose genome is made of RNA, and it cannot replicate directly. Instead, it is supposed to use reverse transcriptase to make DNA corresponding to its RNA and insert that into the cell’s genome. It is activated only when the cell decides to divide.
      DNA viruses and RNA retroviruses are entirely different in their behavior.

      • lukas said

        Prof Bauer,
        even if as you say the mechanism differs between retrovirus and hepatitis virus there is strong evidence that hep virus might be harmless too.I quote now prof. Duisberg (paragraph from hepatitis B virus-liver cancer hipothesys-inventing the aids virus-page 114)”Hoping to rescue the virus hipothesis,scientist resorted to an old favourite among cancer explanations:Perhaps the tumor could result from cells in which the virus DNA accidentally combines with a specific gene of the cell to produce a cancerous mutation.But follow up investigations showed that the pieces of viral DNA did not affect any consistent part of the cell’s genetic structure and that most of them were biochemically dead and therefore not producing any viral protein”.What is valid for hiv is valid for hep b.Cancer arose according to him by a single cell mutation,there is no reasons why the others cell infected remain normal.He says that some kind of chronic inflamation may trigger a mutation in a single cell,but this does not happen most time as the body “get rid of the virus”.That’s why there exist lots of perfect healthy hep b carriers,and contrary people who never encontered the virus who will be affected by liver cancer(mutations are casual)And for the ones who suffer from the chronic hep b(the ones at risk to develop liver cancer),there is no reason to believe they are affected by some particular strain etc,but the cause of the inflamation should be investigated in the lifestyle of the affected,supposed hep b to be a 30 years more latent disease.So say that hep b carriers will develop liver disease is not less dogmatic than to say that hiv pos will develop aids,and as conclusion the similarity is that neither liver disease or aids are contagious.

      • Henry Bauer said

        I think the comparison of Hep B with HIV doesn’t add anything to understanding either of them.

  7. Benedetto said

    Is it so important to figure out the exact patological mechanism by which hiv is supposed to kill the CD4 T cells? what about other viruses? Do we know the patological mechanism for every known infectuos disease?

    • David Crowe said

      Benedetto, if we don’t know HOW ‘a’ causes ‘b’, we don’t know IF ‘a’ causes ‘b’. A description of the method of production of illness (pathogenesis) is part of the proof of causation. Or at least it should be. Virologists routinely evade Koch’s postulates (not just for HIV). If ‘a’ (HIV) caused ‘b’ (low CD4 counts) then there should be a strong correlation between, for example, viral load (HIV) and CD4 counts. But there isn’t a strong correlation. Which means they are not related and therefore ‘a’ probably doesn’t cause ‘b’ (or, perhaps viral load tests don’t measure HIV, which would cause its own problems for HIV theory).

      • Benedetto said

        Yes, I agree but.. .. but, AT LEAST, has anobody ever seen CD4 cells dying in a “hiv infected” colture????

      • Henry Bauer said

        What’s in an “HIV infected”culture? According to Montagnier, the only pathogen is a mycoplasma. But you evade the point about correlation not being causation, and that “how” is also “if”

      • Benedetto said

        Henry. I agree with you that the burden of the proof is theirs and correlation is not causation.. but what I was trying to say was that knowing the pathological mechanism is not essential to understand if a virus is the cause of a certain disease. Koch postulates docet, don’t they? (you can well establish that a virus is the culprit without knowing this biological information, can’t you?) but as far as I know even the Koch postulates have their limits..I mean, their fulfillment is necessary but not always sufficient (the virus that fulfills those postulates could well not be the sole cause, but a cofattor).. so, generally speaking, what instruments/procedures science has nowadays to establish that a virus is responsible for a disease?

      • Henry Bauer said

        Knowing the mechanism seems to me the only conclusive proof.
        Koch’s postulates are an attempt to set out evidence that is NEARLY as good as that, but still there’s room for doubt left. A good discussion, from the early days of “HIV/AIDS”, is by Alfred Evans, “Does HIV cause AIDS? A historical perspective”, Journal of Acquired Immune Deficiency Syndromes, 2 (1989) 107-13

      • lukas said

        For Benedetto:Two exemples of correlation between low cd4,sickness and hiv negative people , and yes i had read that low cd4 counts might matches many illnesses independently by any retroviral infection.

    • Henry Bauer said

      What concerns other viruses is irrelevant. The onus of proof is on those who make claims. The mainstream claims, asserts, that HIV kills CD4 cells. Many pieces of evidence have been put forward, and not contradicted, that it is impossible for HIV to kill CD4 cells: because it is present in so few of them that the normal rate of generation of new cells can easily counteract any losses; that no retrovirus can act in this way (Duesberg’s long, fully documented article); that there are many HIV+ people who remained healthy for decades; etc., etc. — see The Case Against HIV.

      So the burden of proof is on the mainstream to demonstrate that HIV does kill CD4 cells, and that can be done only by discovering the mechanism, because the present cliam is only based on a partial CORRELATION between HIV+ and lowered CD4. Correlation NEVER proves causation; and in this case, it is known that many diseases are associated with lowered CD4 counts in the blood.

      • lukas said

        I’ve read that low cd4 cells count is related much more to the “immunoactivation” response rather than viral load concept.What i wonder is:do people who is hospitalized with any of 40 or more conditions that belong to aids but are hiv negative have low cd4?Does exist a study on sick people that shows that low cd4 is related in general to a condition of sickness indepently by hiv status?If so do negative people who is sick and recovery when treated traditionally for the manifest illness shows also an increase of the cd4 cells?As i intend modern medicine targets hiv as have seen evidence that hiv people don’t recovery brilliantly as the negative if treated traditionally.Is this a prejudice or the truth?And lastly is there a study on negative people who have very low cd4 and stay fine,and are not pushed to be treated as considered healthy?If there exist,are they considered at risk to develop any disease?

      • Henry Bauer said

        It’s never been shown that low CD4 counts denote illness. Among healthy people, there is an enormous range of CD4 counts. They vary with age, time of day, race, and who knows what else. For example (Amatya et al., Clinical Immunology, 112 [2004] 290-5) for 18-25 year-olds the range was 306-1293, mean 700, standard deviation 270 — so about 1/6, say 15%, were less than 430. In other words, something like 20% of young healthy people have CD4 counts below 500, which is a common criterion for giving antiretroviral drugs to HIV+ people.
        CD4 counts became enshrined as indicative of “AIDS” only because Dr Gottlieb, who saw the first patients, happened to have just gotten instruments to count immune-system cells, and there existed no reference data for healthy people.

      • Benedetto said

        Lukas: I think you have a point: knowing if “also” hiv negative people who came down with one of the 29 diseases ascribed to aids have low cd4 counts would be the final nail for this surrogate marker (If at all, to me, it would demostrate once and for all that low cd4 can be a mere consequence and not the cause of illness). Unfortunately – I guess – that nobody bothers to measure those cells in hiv negative patients so we are left without such an information.. (intersting enough, when such a measurement was made and found low cd4 even in negatve people they came up with a new syndrome: ICL, the Idiopathic cd4 Linfocitopenia … only to save the viral theory?)

      • David Crowe said

        There’s actually quite a bit of measurement of CD4 counts in HIV-negative (or, at least, untested) people. Check the material at:

  8. David Crowe said

    Benedetto, they grow “HIV” in CD4 cells. That seems like another conundrum, that the cells that HIV targets (supposedly) for death, are the ones that grow immortally and allow HIV to also flourish. There are many reasons for things to die in culture. How would you know that the cells dying had HIV in them (and that it was the cause of death) when HIV is also found in other cells that aren’t dead. If this wasn’t the case then HIV would rapidly die out in culture as it killed all its hosts. And if CD4 cells grow, even in a cell culture, faster than HIV can kill them, how could HIV deplete CD4 cells in vivo?

    • Benedetto said

      David, I agree with you: finding dying cd4 cells in a colture doesn’t necessary imply they are being killed by a new virus, let alone by hiv, and that “growing the hiv” in such a colture may constitute a contradiction in terms, but I thought that the secret of the Gallo’s colture is to use cancerous cells whose extemely high rate of reproduction allows the reach of a balance between newly formed and dying cd4 cells, making the colture immortal even in presence of a deadly virus.. it sounded reasonable to me..

      • Henry Bauer said

        NOTHING Gallo has done should seem reasonable, or at last sound, to anyone.

      • Benedetto said

        unfortunately his cell line is sold everywhere.. it seems that most of the reserchers don’t think it to be a conundrum …and I wanted to know why

      • Henry Bauer said

        Contemporary science doesn’t pay attention to the scientific facts. Read my Dogmatism in Science and Medicine: How Dominant Theories Monopolize Research and Stifle the Search for Truth, Jefferson (NC): McFarland 2012

  9. K. Lee said

    know we know how hiv causes aids(or so they think), ….more about aptosis …. and drugs

    even david rasnick commented.(funny comment)

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