HIV/AIDS Skepticism

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

HIV protects against cancer and cannot cause AIDS

Posted by Henry Bauer on 2009/12/01

That startling information was disseminated this week by Ruggiero, Punzi, Morucci and Pacini at the Annual Congress of the Italian Association of Cell Cultures (Italian branch of the European Association). A pdf of the program booklet is here; the Ruggiero abstract is at p. 17.

An HIV protein, VpR, detectable in the serum of HIV patients, “induces selective killing of rapidly dividing cancer cells”. HIV has been present in humans since at least the early 1900s and can hardly be responsible for AIDS, which first appeared around 1980. That, together with the cancer-killing propensity of the HIV protein VpR, suggests that a symbiotic relationship had been established between the human genome and HIV. In recent years, however, the tumor-killing activity of VpR may have been masked by the carcinogenic effect of HAART.

From Congress website:
1. Title of Ruggiero et al. presentation
2. Abstract
3. Full poster
4. Theme of Congress (Cell Death: physio-pathological and therapeutic implications) and sponsorship.
The meeting was hosted by the University of Firenze and sponsored also by the Ordine dei Medici, the only official organization that represents medical doctors and surgeons in Italy. Phoenix Foundation is a non-profit (“onlus”).
Since the full poster is too small to read from this screen shot, here is an easily readable version. Like the other presentations at the Congress, it had been accepted only after peer review.


This complete documentation is provided because of the penchant AIDS groups and vigilantes have amply displayed in their attempts to denigrate or hide the overwhelming evidence that disproves HIV/AIDS theory. The Ruggiero presentation was accepted after peer review at a mainstream conference sponsored by impeccably authoritative institutions.


The presentation by Ruggiero et al. not only brings the stunning news that “HIV” is protective against cancer, it also confirms the conclusion, perhaps most recently expressed by Montagnier, that HIV is readily fended off by robust immune systems: HIV is a passenger virus, a consequence and not a cause of immune deficiency.

This work reminded me of the suggestion by James Graham that the evolution of mechanisms for warding off cancer may have been crucial elements in the evolution of animals: see Graham’s website.

17 Responses to “HIV protects against cancer and cannot cause AIDS”

  1. Cytotalker said

    A few months ago, I felt I sounded certifiably insane for using the term “protective” to describe HIV’s VPR protein in a title for a blog entry I wrote, but the evidence was clear, and I went ahead and rather nervously clicked on that publish button. In this case, VPR protects against lethal bacterial endotoxin, with CD4 cells, in particular, benefiting from such protection.

    With mounting evidence of such protective roles of HIV also emerging against cancer, the evolving scenario is that of the medical-pharmaceutical complex committing a gross act of malpractice by in principle pursuing, by means of HAART, the suppression of the body’s own protective mechanisms from carcinogenic or infectious stressors, all because an ambitious and dishonest scientist from the eighties sought to indict said protective mechanisms as the cause of AIDS.

    • Henry Bauer said

      Cytotalker: MANY THANKS for that fascinating information with the link to the 2005 [!!] article.

      • Cytotalker said

        Thanks for bringing attention to the findings of Ruggiero et al. Aside from the major blow landed on the HIV/AIDS hypothesis, it is also a relief to the millions of HIV positives who may read this and find out that their condition, rather than being one for which they should feel shameful, impure, or condemned, is instead one involving the marvelously complex mechanisms of the organism in its much ignored ability to heal itself.

        One day, doctors — rather than artificially halting this epigenetic process of adaptation to stressors — will know enough to wonder how instead they could assist the organism in its own symbiotic regenerative process. Findings such as that of Ruggiero et al. may eventually lead views on HIV to evolve as did those on tonsils, which not so long ago were deemed as nuisance or even harmful body parts to be extracted but whose role in immunity is today increasingly recognized. The physiological role of elevated cholesterol as an important adaptation to stress seems to be embarking on the same path, one that is highly unprofitable to those who sell treatments for this so-called pathology.

      • Henry Bauer said

        Cytotalker: Yes indeed. An excellent review of some of the areas where medicine is on the wrong track is “Malignant Medical Myths” by Joel Kauffman, who has religiously searched the literature to uncover what the facts really are about, say, daily aspirin for heart health, statins to lower cholesterol, blood-pressure drugs, and more. Sometimes the mainstream belatedly catches up with Kauffman, as in the recent announcement that annual mammograms are not a panacea.

  2. Henry,

    Is there any reason why you spoil the orthodoxy’s ongoing propaganda efforts in vivo on World Anti-Cancer Day?

    DISCUSSION. These data could be interpreted as follows: on one hand, HAART itself might be involved in the development of cancer, in particular lung cancer, and may not have a beneficial effect on either the incidence or outcome of the lung cancer (…). On the other hand, HAART-induced reduction of viremia could decrease HIV-associated anti-tumor activity (p. 48 of the booklet).

    Kind of embarrassing, isn’t it?

  3. Tony Lance said

    It’ll be interesting to see how the AIDS Truthers address this one.

    Also, it’s remarkable to me how quite different lines of dissident thought keep coming to the same conclusion, more or less, that “HIV” is an effect or consequence of immunodeficiency and not a cause.

    • Guy Harris said

      More accurately, having a positive reaction to the non-specific HIV test. The body is trying to defend against something, but we don’t quite know what.

      • Henry Bauer said

        Guy Harris: A positive “HIV” test need not even mean that there’s a defense reaction. About 15% of healthy blood donors light up the p24 band, and p41 has also been found in blood platelets of healthy individuals: Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. Has Gallo proven the role of HIV in AIDS? Emergency Medicine [Australia] 1993;5:113-123.

  4. Dear Henry,

    Thank you for running this blog and for all your help with our work. I wish to answer to some of the comments on our work presented in Firenze, Italy, last week.

    Cytotalker: I felt just the same (certifiably insane) a few months ago when I began to realize the anti-cancer role of HIV. However, the “orthodox” evidence is so solid that we cannot ignore it. As a cancer researcher, however, I already knew that known pathogenic bacteria (in particular anaerobia) have been proposed as anti-cancer agents. Thus, the case of HIV is not isolated (absit iniura verbis about HIV isolation). Furthermore, I was moved by your words ” … it is also a relief to the millions of HIV positives who may read this and find out that their condition …”. The point, however, is to let these people know. We, as scientists, are doing our best by publishing our results and presenting them to authoritative congresses, but I doubt that “the millions of HIV positives” read conference abstracts. Thus we need the help of everybody to let people know.

    Tony Lance: “It’ll be interesting to see how the AIDS Truthers address this one”. I did not receive any comment on their part. All the comments at the conference were highly positive and all the authorities there (academic, medical and military) were positive and encouraging. I doubt that we shall hear any comment by AIDS Truthers: all the references come from mainstream orthodox journals. The work was peer reviewed and accepted. It cannot be withdrawn (the congress is over and the communications published). I think that this time they will have to accept it.

    Again, I thank you all for your comments.

    Marco Ruggiero

    • Gene said


      “HIV” neither ptotects or destroys – it’s an experimental artifact.

      So it’s a fundamental error IMO to call vpr an “HIV protein” because it’s never been demonstrated that “HIV proteins” are specific to a virus (i.e., an elementary copying machine that “hijacks” the machinery of a cell).

      Like all cellular genes, vpu is pleiotropic.

      The HIV experts claim that vpr (gene at nucleotide positions 5619 to 5850 of Gallo’s HXB2 clone, ref 1), is essential for transporting the “pre-integration complex” into the nucleus. (2,3)

      Or NOT, per the usual, they contradict each other. According to others cited by Popov et al: “Vpr is not required for import under all circumstances.” (2)

      From Popov et al (2):

      “A discrepancy between the absolute requirement for Vpr in our in vitro nuclear import system and an apparently non-essential role of this protein in some in vivo settings may be explained by the presence of putative cellular analogues of Vpr.”

      “Existence of such proteins is also suggested by the amazing conservation of the Vpr binding site(s) on a karyopherins from such distantly related species as yeast and humans.”

      From Dettenhofer and Yu (3):

      “It has been suggested that vpr … (is) serving as a global transactivator”; (meaning the equivalent of cellular NFkB).

      Amazing indeed when the HIV experts find so many documented cellular functions of a so-called HIV protein, like causing apoptosis. Also amazing, because HIV experts now admit to the presence of cellular proteins in “purified virions”.

      BTW, Did Gallo check this specific 230 bp fragment of his HXB2 clone against cellular DNA? It appears from the record that he didn’t.

      The record also shows hybridization of larger fragments of “HIV genome” to cellular DNA, including the env region, by subsequent research. Specific hybridizations were found close to the region of the “HIV genome” where vpr “resides”.


      1. Calugi et al; Journal of Virology, Dec 2006, V80:11892-11896

      2. Popov et al; The EMBO Journal Vol.17 No.4 pp.909–917, 1998

      3. Dettenhofer & Yu; Journal of Virology, Feb 1999, V73:1460-1467 (These good folk use a weasel word, it “enhances the nuclear import of the preintegration complex”.)

      • Gene,

        Thank you for the information. One question: do you know whether is there any recent news about the putative cellular analogues of Vpr?



    • “It is also a relief to the millions of HIV positives who may read this and find out that their condition …”. The point, however, is to let these people know. We, as scientists, are doing our best by publishing our results and presenting them to authoritative congresses, but I doubt that “the millions of HIV positives” read conference abstracts. Thus we need the help of everybody to let people know.”

      Some HIV-positive people are reading things like that🙂 Thank you, for you work, Dr. Marco Ruggiero! And all other scientists that talk against HIV=AIDS, everything you say is very important for us – HIV-positives.
      I am an HIV-positive female, I had cervical erosion several years ago. It’s not cancer but I heard it can lead to it. After my HIV+ diagnosis I went to my gynecologist and she checked and told me that this erosion was self-eliminated by the good immune response of my body (she didn’t know about my HIV+)🙂
      The same thing happened with my another HIV+ female friend. We both are not taking HAART.


  5. Gene said

    Good question.

    A “cellular analogue” is heat shock protein 70.

    Here’s more from above reference 2:

    “Existence of such proteins is also suggested by the amazing conservation of the Vpr binding site(s) on a karyopherins from such distantly related species as yeast and humans. One of the possible candidates for this role is the heat-shock protein 70 (Hsp70, Hsc70), which can perform functions similar to those of Vpr. Hsp70 has been shown to facilitate the interaction between the NLS and karyopherin a (Shulga et al., 1996; Nadler et al., 1997); the ectopic expression of human Hsp70 in mouse cells complements the defective import of a mutant SV-40 large T antigen (Jeoung et al., 1991), and the depletion of Hsp70 from cytosolic extracts prevents import (Shi and Thomas, 1992; Okuno et al., 1993). It seems likely that cellular Vpr-like
    proteins may function to enhance nuclear import in some cells in response to certain stimuli.”

    HSPs* are also known as “stress proteins”, associated with oxidative stress, and turning up in “lentiviruses”.

    Here’s an interesting paper that deals with incorporation of specific cellular protein families into HI virions.

    KOLEGRAFF** et al; Characterization and Role of Lentivirus-Associated Host Proteins. Experimental Biology and Medicine 231: 252-263 (2006)

    They include transport/cargo proteins VPS28 and VPS4B in HIV column of Table 1: “Host Antigens Incorporated into the Virions of Some Enveloped Viruses”. Some of this cellular-protein incorporation is because the virion envelope is made up “from the components of host membranes”. These components include cell surface receptors CD2, CD3, CD4, CD8, CD11, CD14, CD19, CD25, CD30, CD44 and CD48.

    The list includes signal transduction adhesion molecules, etc.

    This collapses the argument, I think, for spending any more taxpayer dollars on failed anti-HIV vaccination federal research program. The program’s a waste and should be ground to a screeching halt; too many other worthy projects need funding.

    But heat shock proteins associated with apoptosis and cancer cells strikes me as worthwhile area. I’ve seen news reports of researchers looking into HSP’s and effective cancer vaccinations.

    Of interest perhaps (Kolgraff et al), there’s such a thing as: “HIV Release from Macrophages via Exosomes”, second “exit strategy” besidesa the one used in T-cells (the “classical pathway”).

    *Heat shock proteins 60, HSP 70 and HSC 70 are in HIV column of Table 1 of Kolgraff et al.

    **Department of Pathology and Laboratory Medicine,
    Emory University School of Medicine,
    Atlanta, Georgia 30322

  6. How interesting that “HIV’s” Vpr from “tat part” makes some anti-cancer actions which are p53-independent from “good” p53, this one:

    And in the same time “HIV” has another, his own p53 (“bad”) from “gag part” as indicated here:

    How can be those two p53? may be there is some mixture between them? And the most interesting question : how can test Western Blot, or any other HIV test, determine whether this p53 is bad one, or good one? As “good” p53 which is tumor supressor also has his own monoclonal antibodies:

    As far as I know, Western blot determine proteins only by their molecular weight. So instead of “catching” “HIV reverse transcriptase or other HIV’s proteins, WB can catch this good p53 protein and his antibodies. And what will happen if thinking you are lucky inhibiting “HIV” with those HAART RT, protease and intergrase inhibitors, you are going to inhibit p53 who are “the guardian of the genome”, the “guardian angel gene”, and the “master watchman”???! I was asking this question to some AIDS-experts online and I didn’t get any answer.

  7. It just gets crazier by the day. You claim HIV doesnt exist , there certainly are no tests that can detect or diagnose HIV , THEN in the next breath you talk as if it does exist. Do you know how rediculous you all sound ?

    Andy Lindsay.

    • Henry Bauer said

      Andy Lindsay:
      It’s very difficult to write concisely. I have to use the term that is in general use. Perhaps I should put “HIV” everywhere, as a short-hand for “what is described as HIV, but which doesn’t exist, and really is whatever an ‘HIV’ test happens to detect”. In my book, I used F(HIV) as denoting the frequency of HIV tests so that I wouldn’t have to keep explaining.
      What’s ridiculous — and tragic — is that the mainstream keeps referring to a non-existent entity and administering toxic drugs to people who happen to test positive on an entirely non-specific and misleading test.

    • KC Blair said

      I agree with you, Andy.

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