HIV/AIDS Skepticism

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

HIV is good for you: protects against cancer

Posted by Henry Bauer on 2011/02/04

“HIV protects against cancer and cannot cause AIDS” (2009/12/01) reported on a paper presented at the Annual Congress of the Italian Association of Cell Cultures by Ruggiero, Pacini, et al.: the HIV protein, VpR, induces selective killing of rapidly dividing cancer cells.

This pointed to a possibly symbiotic relation between HIV and the human genome, the anti-cancer action of HIV causing it to be selectively favored by evolutionary processes.
That evolution of mechanisms for warding off cancer may have been crucial elements in the evolution of higher organisms had been postulated also by James Graham.
Now there comes further support for this from an independent source. Hessol et al., “HIV tropism and decreased risk of breast cancer” [PLoS One, 16 December 2010, 5(12):e14349],  found that “breast cancer risk was significantly lower for women with human immunodeficiency virus (HIV) infection compared to the general population. This deficit in HIV-associated breast cancer could not be attributed to differences in survival, immune deficiency, childbearing or other breast cancer risk factors” . It seems that “Low breast cancer risk with HIV is specifically linked to CXCR4-using variants of HIV”.
This is a different mechanism than that found by Ruggiero et al. Perhaps that explains why Hessol et al. don’t cite them or Graham, but a more probable reason is the explosive growth of publications about cancer and HIV, which makes it all but impossible to remain aware of all potentially relevant research.

8 Responses to “HIV is good for you: protects against cancer”

  1. John Samson said

    Well, I’ll be,,,that’s the next NEW treatment for Cancer they will be selling to the public.

    • Henry Bauer said

      John Samson:
      Sure, why not? All the wonder drugs of the last few decades have more-or-less serious “side” effects, so it’s always a matter of weighing benefits against risks. One of my friends took marvelous eye drops that reduced the pressure in his eyes magnificently, but at the cost of a rash all over his body that’s taken weeks of steroid treatment to overcome. Several of my senior friends have mentioned loss of feeling in their feet, and in response to my question, all of them turn out to have been taking statins, one of whose known “side” effects is peripheral neuropathy. And so on.

      • Robin said

        Henry, at risk of being too cynical and unkind, a silver lining of what we might now call hoax medicine has been that it has a eugenic effect, killing off intellectually deficient distinguished professors and leaving the merely independent-minded discards of the system still standing?

      • Henry Bauer said

        It kills off innocent pateints, not the deluded professors.

  2. mo79uk said

    I’ll be damned…An antibody that’s good for you. 🙂

    Recently my girlfriend’s cat died of multiple facial tumours but the death was attributed to FIV, which again is only detected by the presence of antibodies. Is it correct to suggest that vets might be failing to look for exact causes once *IV positivity is detected? I’m guessing that most *IVs are based on the HIV model.

    Also, on March 13, there’s a special screening of House of Numbers in London hosted by the IRF – just thought I’d share:

  3. Jean Umber said

    Let me stress the importance of the chemistry of derivatives of nitrogen to understand what AIDS.
    Cell death is caused by the destruction of the membrane during the nitration of tyrosine under the influence of peroxynitrite. Too excessive reduction leads to the disappearance of peroxynitrite. The destruction of cancer cells is hampered by a too reducing medium and cancer can develop.

    HIV, which I think is only a marker of AIDS, only appears if the presence of peroxynitrite.

    Click to access 1742-4690-4-76.pdf

    These are the real culprits of AIDS, coming from the decomposition of poppers, drugs amino, certain antibiotics, nitrogen, AZT, using Viagra, occurring if the blood selenium levels are too low as in Southern Africa.

    Thus, when the amount of P24 is high, the destruction of cancer cells is rapid.

    Logically, antiretrovirals are all good reducing agents (epivir, tenofovir), and thus promote cancer by preventing peroxynitrite to destroy diseased cells.

    This is why druged patients are dying of cancer now.

  4. HGY said

    See if you can put this Vpr-related narrative together…

    J Virol. 2006 Nov;80(21):10407-18. Epub 2006 Sep 6.

    Human immunodeficiency virus type 1 Vpr induces DNA replication stress in vitro and in vivo.

    Zimmerman ES, Sherman MP, Blackett JL, Neidleman JA, Kreis C, Mundt P, Williams SA, Warmerdam M, Kahn J, Hecht FM, Grant RM, de Noronha CM, Weyrich AS, Greene WC, Planelles V.
    Division of Cellular Biology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah 84132, USA.

    The human immunodeficiency virus type 1 (HIV-1) viral protein R (Vpr) causes cell cycle arrest in G2. Vpr-expressing cells display the hallmarks of certain forms of DNA damage, specifically activation of the ataxia telangiectasia mutated and Rad3-related kinase, ATR. However, evidence that Vpr function is relevant in vivo or in the context of viral infection is still lacking. In the present study, we demonstrate that HIV-1 infection of primary, human CD4+ lymphocytes causes G2 arrest in a Vpr-dependent manner and that this response requires ATR, as shown by RNA interference. The event leading to ATR activation in CD4+ lymphocytes is the accumulation of replication protein A in nuclear foci, an indication that Vpr likely induces stalling of replication forks. Primary macrophages are refractory to ATR activation by Vpr, a finding that is consistent with the lack of detectable ATR, Rad17, and Chk1 protein expression in these nondividing cells. These observations begin to explain the remarkable resilience of macrophages to HIV-1-induced cytopathicity. To study the in vivo consequences of Vpr function, we isolated CD4+ lymphocytes from HIV-1-infected individuals and interrogated the cell cycle status of anti-p24Gag-immunoreactive cells. We report that infected cells in vivo display an aberrant cell cycle profile whereby a majority of cells have a 4N DNA content, consistent with the onset of G2 arrest.

    Click to access Bird.pdf

    Immunity, Volume 9, Issue 2, 229-237, 1 August 1998

    Helper T Cell Differentiation Is Controlled by the Cell Cycle

    Jennifer J Bird1, 3, Daniel R Brown3, Alan C Mullen3, Naomi H Moskowitz1, 3, Michael A Mahowald1, 3, Jenny R Sider1, 3, Thomas F Gajewski1, 2, Chyung-Ru Wang2, 3 and Steven L Reiner1, 3, 4, ∣∣, *,
    1 Department of Medicine, Committee on Immunology, The University of Chicago, Chicago IL 60637, USA
    2 Department of Pathology, Committee on Immunology, The University of Chicago, Chicago IL 60637, USA
    3 Gwen Knapp Center for Lupus and Immunology Research, Committee on Immunology, The University of Chicago, Chicago IL 60637, USA
    4 Committee on Developmental Biology, Committee on Immunology, The University of Chicago, Chicago IL 60637, USA


    Helper T (Th) cell differentiation is highly regulated by cytokines but initiated by mitogens. By examining gene expression in discrete generations of dividing cells, we have delineated the relationship between proliferation and differentiation. Initial expression of IL-2 is cell cycle-independent, whereas effector cytokine expression is cell cycle-dependent. IFNγ expression increases in frequency with successive cell cycles, while IL-4 expression requires three cell divisions. Cell cycle progression and cytokine signaling act in concert to relieve epigenetic repression and can be supplanted by agents that hyperacetylate histones and demethylate DNA. Terminally differentiated cells exhibit stable epigenetic modification and cell cycle-independent gene expression. These data reveal a novel mechanism governing Th cell fate that initially integrates proliferative and differentiative signals and subsequently maintains stability of the differentiated state.

    Nature. 2002 May 2;417(6884):95-8.

    HIV preferentially infects HIV-specific CD4+ T cells.

    Douek DC, Brenchley JM, Betts MR, Ambrozak DR, Hill BJ, Okamoto Y, Casazza JP, Kuruppu J, Kunstman K, Wolinsky S, Grossman Z, Dybul M, Oxenius A, Price DA, Connors M, Koup RA.
    Vaccine Research Center, NIAID, NIH, Maryland 20892, USA.


    HIV infection is associated with the progressive loss of CD4(+) T cells through their destruction or decreased production. A central, yet unresolved issue of HIV disease is the mechanism for this loss, and in particular whether HIV-specific CD4(+) T cells are preferentially affected. Here we show that HIV-specific memory CD4(+) T cells in infected individuals contain more HIV viral DNA than other memory CD4(+) T cells, at all stages of HIV disease. Additionally, following viral rebound during interruption of antiretroviral therapy, the frequency of HIV viral DNA in the HIV-specific pool of memory CD4(+) T cells increases to a greater extent than in memory CD4(+) T cells of other specificities. These findings show that HIV-specific CD4(+) T cells are preferentially infected by HIV in vivo. This provides a potential mechanism to explain the loss of HIV-specific CD4(+) T-cell responses, and consequently the loss of immunological control of HIV replication. Furthermore, the phenomenon of HIV specifically infecting the very cells that respond to it adds a cautionary note to the practice of structured therapy interruption.

    J Exp Med. 2003 Dec 15;198(12):1909-22.

    HIV-1 viremia prevents the establishment of interleukin 2-producing HIV-specific memory CD4+ T cells endowed with proliferative capacity.

    Younes SA, Yassine-Diab B, Dumont AR, Boulassel MR, Grossman Z, Routy JP, Sekaly RP.
    Département de Microbiologie et Immunologie, Université de Montréal, 2900 Edouard-Montpetit Boulevard, Montréal H3T 1J4, Canada.


    CD4+ T cell responses are associated with disease control in chronic viral infections. We analyzed human immunodeficiency virus (HIV)-specific responses in ten aviremic and eight viremic patients treated during primary HIV-1 infection and for up to 6 yr thereafter. Using a highly sensitive 5-(and-6)-carboxyfluorescein diacetate-succinimidyl ester-based proliferation assay, we observed that proliferative Gag and Nef peptide-specific CD4+ T cell responses were 30-fold higher in the aviremic patients. Two subsets of HIV-specific memory CD4+ T cells were identified in aviremic patients, CD45RA- CCR7+ central memory cells (Tcm) producing exclusively interleukin (IL)-2, and CD45RA- CCR7- effector memory cells (Tem) that produced both IL-2 and interferon (IFN)-gamma. In contrast, in viremic, therapy-failing patients, we found significant frequencies of Tem that unexpectedly produced exclusively IFN-gamma. Longitudinal analysis of HIV epitope-specific CD4+ T cells revealed that only cells that had the capacity to produce IL-2 persisted as long-term memory cells. In viremic patients the presence of IFN-gamma-producing cells was restricted to periods of elevated viremia. These findings suggest that long-term CD4+ T cell memory depends on IL-2-producing CD4+ T cells and that IFN-gamma only-producing cells are short lived. Our data favor a model whereby competent HIV-specific Tcm continuously arise in small numbers but under persistent antigenemia are rapidly induced to differentiate into IFN-gamma only-producing cells that lack self-renewal capacity.

    • Henry Bauer said

      HGY and all readers:
      I defer the task to molecular biologists and those who believe that HIV may exist as an endogenous infectious agent.

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