HIV/AIDS Skepticism

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


Posted by Henry Bauer on 2008/01/15

Etienne de Harven, MD, is Emeritus Professor of Pathology, University of Toronto; he has been a member of the Sloan Kettering Institute (New York) and was on the AIDS Advisory Panel set up by President T. Mbeki in 2000. He has special expertise in electron microscopy; already 4 decades ago he published electron micrographs of the Friend leukemia virus.

On 8 December 2003, he addressed the European Parliament on “Problems with isolating HIV”. That address has never previously been published in English, and I’m delighted and honored that he was willing to have it posted here. Professor de Harven’s contact information is:
“Le Mas Pitou”, 2879 Route de Grasse, 06530 Saint Cézaire, France;
e-mail; Tel or Fax (33) 4 93 60 28 39



How can we best help Africa? How can we set priorities aimed at bringing under control what is described as an AIDS epidemic? For twenty years, all AIDS research has been based on the HIV hypothesis. Do we now have reasons to question this hypothesis? Yes, because there is a major problem with isolation and purification of HIV. The major problem being that, in spite of innumerable claims to the contrary, this retrovirus has never been isolated nor purified in a scientifically acceptable manner that would satisfy the classic requirements of virology.

To demonstrate the problem’s magnitude it appears necessary to compare current results on HIV with those obtained, previously, in experimental pathology, on another retrovirus known to be significantly associated with a particular leukaemia of laboratory mice, the Friend leukaemia. Both retroviruses, i.e. the Friend leukaemia virus and the HIV hypothetically related to AIDS, share extremely similar morphology under the electron microscope, have identical diameters, and sediment at the same density in sucrose gradients. A direct comparison between isolating and purifying these two different retroviruses is, therefore, entirely appropriate.

Mice suffering from the Friend leukaemia have considerable numbers of retroviral particles in their blood stream. This phenomenon, described as “viraemia“ in the past (1), would be called “viral load“, in today ’s terminology. From only a few ml of the blood plasma of leukaemic mice, the viral particles could be readily separated by a simple technique of ultrafiltration, then sedimented by high-speed centrifugation and finally prepared for electron microscopy. The results are illustrated in the first slide.


On this electron microscope image, a uniform population of virus particles is clearly recognized. They all have the same diameter and morphology, and one has to look very carefully to identify rare, non-viral structures, attesting to the high degree of purification of these retroviral particles. Such samples of purified retrovirus were successfully used to identify viral proteins and to extract viral RNA. The method applied to achieve this purification of a typical retrovirus is rapid, inexpensive and highly reproducible.

Most surprisingly, nobody has ever succeeded in demonstrating HIV particles in the blood of any AIDS patient by this simple method, even though patients were selected for presenting a so-called high “viral load” as determined by PCR methods. This embarrassing lack of electron microscope evidence for substantiating the nature of the so-called viral load in AIDS patients was first reported during an important AIDS conference that took place in Pretoria, S.A., in May 2000 (2). None of the AIDS experts present at that conference could demonstrate the presence of retroviral particles in the blood of AIDS patients. Moreover, almost two years ago, a substantial award ($100,000) was officially offered (3) to anybody who would demonstrate HIV particles in the blood of allegedly high viral load patients. Two years later, the award has still not been claimed. Obviously, what was so readily and reproducibly demonstrated in leukaemic mice has never been observed in any AIDS patient.


Over the past 20 years, the medical literature has been inundated with innumerable papers, attempting to dodge the lack of electron microscope evidence for the presence of retroviral particles in samples directly collected from AIDS patients. In all these papers, the missing retroviral particles have been swiftly substituted with so-called HIV “markers”. These “markers” were of physical, biochemical, or genetic nature.

Physical markers.
As known for a very long time, classic retroviruses identified in chicken, mice and cats, all share the same shape and density, and therefore sediment at exactly the same level during high-speed centrifugation in sucrose gradients. Actually, they all sediment at the density of 1.16 gm of sucrose per ml (4). The alleged HIV being classified as a retrovirus, it was logical to expect it to sediment at that same density.
However, as was also well known years before the emergence of AIDS, a large variety of cellular fragments and debris also sediment at that density (5, 6). Collecting material sedimenting at that density does not, therefore, demonstrate the isolation of retroviruses, unless a careful control by electron microscopy rules out any contamination by cellular debris. The importance of these essential controls was stressed during a conference that took place in Paris, in 1973 (4). Most surprisingly, in the same laboratory of the Pasteur Institute, then years later, in 1983, a paper was published (7), in which these controls were missing. It appeared later (20), however, that these controls were attempted but gave discouraging results. Still, in the title of that paper, “isolation” of a new retrovirus, the future HIV, was announced. Dramatically enough, this is the paper that placed AIDS research on highly questionable tracks for the following two decades.

Biological markers.
In 1970, Temin (8 ) and Baltimore (9) discovered the activity of a so far totally unexpected enzyme in allegedly purified samples of experimental retroviruses. This enzyme was called “reverse transcriptase” because it induces DNA synthesis from RNA templates. It was indeed a fundamental discovery that revolutionized molecular biology. This enzyme activity was first observed in RNA tumour viruses and was, therefore, initially thought to represent a characteristic “marker” of these viruses which, consequently, received a new name: “retroviruses”. Ever since, reverse transcriptase activity has been used as a “marker” for HIV…

However, shortly after the publications by Temin and Baltimore, it was discovered that reverse transcriptase activity was not restricted to “retroviruses” but was in fact a most common phenomenon in biology (10, 11), as reviewed by Varmus in 1987 (12). Unfortunately, and yet again, Temin and Baltimore omitted to verify the purity of the viral samples on which their observations were made. Consequently, any contamination of these samples by cell, bacterial, or mycoplasma debris could just as well have explained the presence of the reverse transcriptase activity observed by these authors. In 1983, the Pasteur group based their claim for the isolation of a new retrovirus primarily on 1) the detection of reverse transcriptase activity in 2) material sedimenting at the density of 1.16 gm/ml. These two criteria completely lose significance if the data are not verified by electron microscopy to exclude possible interference by non-viral contaminants known to be frequently present in allegedly “purified” retroviruses (5, 6).

Several proteins, allegedly of viral origin, are frequently used as “specific” HIV markers, p24 for example. Doubts concerning its specificity have been expressed for a long time (15). The complete lack of agreement between results obtained with p24 and measurements of “viral load” obtained by PCR were recently stressed (13). Surprisingly, in Western blot tests, 40% of sera from dogs reacted positively with proteins obtained by genetic recombination technology, such as gp120, gp47, p31 and p24 (14). This had to be expected since Eleni Papadopoulos, Val Turner and the Perth Group had initially, extensively demonstrated the total lack of specificity of all the alleged HIV structural proteins in a paper, published 10 years ago in Nature Biotechnology (15), a fundamental paper that was completely ignored. To cite only key examples, gp41 probably corresponds to actin, and gp120-160 are likely oligomers of gp41. Evidently, cell debris contaminating very poorly purified retroviral samples may also readily account for the presence of alleged retroviral markers, and frequently reported “successes” in HIV “isolation” most likely result from faulty reliance on non-specific “markers”.

Genetic markers and measurements of “viral load”.

This approach could seem more attractive for two reasons: 1) it applies directly to a patient’s blood, therefore avoiding all the uncertainties of complex cell cultures, and 2) it is supposed to be a quantitative method.

However, as already stressed, it has never been possible to visualize any retroviral particle by electron microscopy in the blood of AIDS patients, even though these patients are selected for having a so-called very high “viral load” (2). Moreover, it appears very likely that PCR methods amplify small RNA fragments, more frequently observed under conditions of stress and of chronic illnesses (16), and which include retroviral segments originating from human endogenous retrovirus [endogenous = originating within the body, native to the human genome, not from external source]. This is not surprising since about 2% of the human genome has marked homology with the retroviral genome (17). Consequently, “measuring” the “viral load” by PCR methods is likely to have no relationship whatsoever with real quantification of a hypothetical exogenous [having a cause external to the body] HIV viremia. Kary Mullis himself, Nobel Prize laureate for his discovery of the PCR method, categorically rejects the use of “his” method for quantitative measurements of a hypothetical HIV viremia (18 ).

The abuse of… beautiful pictures.

The “viral load” of newspapers and magazines, all over the world is extremely high, meaning the number of pictures of HIV published almost daily in the world’s press. These pictures are extremely attractive, and are frequently rich in artificial colors. They clearly exemplify the danger of misinforming the public with computer graphics. To publish such images brings to the attention of the general public, and of the medical profession as well, an apparently crystal-clear message: “Yes, HIV has been isolated since one can portray it under the electron microscope”.


All these images are computerized rationalizations and embellishments of actual electron microscope pictures similar to those illustrating, for example, Barré-Sinoussi’s paper (7). But not one of these pictures originated directly from one single AIDS patient! They ALL originated from complex cell cultures prepared in various laboratories (19), cultures that have been described as “real retroviral soups” (20). Indeed, everything was done to make sure that retroviral particles (and the celebrated budding forms) would appear in these cultures. Not done were the essential verification experiments that could have clarified the endogenous origin of these viruses. Even if these control experiments were done, their results were apparently never published. We are still waiting for a newspaper that would publish beautiful computer graphics of HIV and would have the honesty to explain to their readers that all these still have to be confirmed with samples originating directly from AIDS patients.

In AIDS research, most of the cell cultures used are mixed and hyper-stimulated.

Mixed, because they contain, for example, lymphocytes from a patient plus the H9 cells from Gallo’s lab, cells well known to be chronic carriers of retroviruses (21). Or, as in the Pasteur Institute case (7), lymphocytes from an AIDS suspected patient plus lymphocytes isolated from umbilical cord blood that originated in the placenta and known since 1979 (22) to be likely to carry human endogenous retrovirus.

These cultures are hyperstimulated with one or two growth factors such as phytohemagglutinin (PHA), T cell lymphocyte growth factor (TCGF), interleukin2, or corticosteroid hormones. All these factors are known to activate the expression of endogenous retroviruses (HERVs), which are defective viruses that may acquire envelopes and bud on the surface of cells activated by these factors. Presumably, this is exactly what happened when cord blood lymphocytes were activated with PHA and TCGF in the Pasteur 1983 experiments (7). Unfortunately, the control experiments needed to verify this interpretation remain to be done.

In short, it seems that electron microscopy was not used when it was essential to demonstrate the absence of contaminating cell debris in allegedly purified virus preparations, and misinterpreted when stimulated cord blood lymphocytes showed budding retroviruses.


Indeed, HIV has never been properly isolated, nor purified, and, consequently, the HIV/AIDS hypothesis has to be fundamentally reappraised (23, 24, 25, 30, 32).

More precisely, without purification of HIV, HIV-specific antigens could never have been rigorously identified (15). Still, so-called HIV antigens are instrumental in all the serological tests allegedly identifying specific HIV antibodies—ELISA, Western Blot, and more recent rapid tests such as “ Capillus”, “Determine”, and “Vironostika”. Recombinant DNA technology for “viral” antigens certainly yields purer products, but fails to make up for the missing specificity. No surprise, therefore, that dozens of different medical conditions, including tuberculosis, malaria, leprosy, multiple blood transfusions, many vaccines, multiparity, etc. all give false-positive “HIV” tests (26).

Retroviral particles have unquestionably been observed, not directly in AIDS patients, but in mixed, hyper-stimulated cell cultures (7). They most likely represent forced expression, in cell cultures, of human endogenous retroviruses (17), whose hypothetical role in the etiology of AIDS has never been proved.

The HIV particles, missing from the patients, have been conveniently substituted by molecular “markers”, because the HIV=AIDS hypothesis had to be saved at all cost (see the Durban Declaration, 27), even at the price of scientific integrity (28 ).

If AIDS were indeed caused by a retrovirus, how can we explain that 20 years of considerable research efforts, based exclusively on that single hypothesis, have failed to isolate the responsible exogenous retrovirus? Twenty years to end up with no curative treatment, no vaccine, and no verifiable epidemiological predictions.

Obviously, time is pressing us to ask courageously the essential question, namely, is the HIV=AIDS hypothesis correct? Because it is entirely possible to view AIDS differently, outside the field of infectious diseases, and outside the field of retrovirology (29). And in this perspective, which is replete with optimistic predictions, all the difficulties encountered in attempted isolation and purification of the hypothetical HIV may find an extremely rational explanation. Indeed, doubts concerning the very existence of HIV are nothing new, and were expressed by several dissident scientists several years ago (30, 31). I completely share these doubts. Let us not forget the title of Peter Duesberg’s book (33) published in 1996: “Inventing the AIDS Virus”.
Consequently, priorities for medical assistance to sub-Saharan Africa should, most urgently, be revised as follows:

— Treat all endemic tropical diseases with their specific treatments.

— Stop all use of antiretroviral drugs until the isolation of HIV and its pathogenicity are scientifically established.

— Stop using highly crossreacting serological tests, the HIV specificity of which is far from demonstrated.

— Provide African people with clean drinking water, proper housing and sanitation, efficient health-care infrastructures, and means to combat malnutrition.

Thank you.

References (the URLs below are no longer active)

(1) de Harven E. Viremia in Friend murine leukemia: the electron microscope approach to the problem. Pathologie-Biologie 1965; 13: 125-134. See also de Harven E., Pioneer deplores “ HIV”, Continuum 1997; 5 #2: 24.
(2) de Harven E. Summary statement. Interim Report of the AIDS Advisory Panel, Pretoria, SA, May 2000. Published by the Government of South Africa, 4 April 2001.
(3) Russel A.
(4) Sinoussi F et al. Purification and partial differentiation of the particles of murine sarcoma virus (MMSV) according to their sedimentation rates in sucrose density gradients. Spectra, #4, 1973, pp 239-243.
(5) Bess JW et al. Microvesicles are a source of contaminating cellular proteins found in purified HIV-1 preparations. Virology 1997; 203: 134-144.
(6) Gluschankof P et al. Cell membrane vesicles are a major contaminant of gradient-enriched human immunodeficiency virus type-1 preparations. Virology 1997; 230: 125-133.
(7) Barré-Sinoussi F. et al. Isolation of a T-lymphotropic retrovirus from a patient at risk for acquired immune deficiency syndrome (AIDS). Science 1983; 220: 868-871.
(8 ) Temin HM, Mizutani S. RNA-dependent DNA polymerase in virions of Rous sarcoma virus. Nature 1970; 226: 1211-1213.
(9) Baltimore D. RNA-dependent DNA polymerase. Nature 1970; 226: 1209-1211.
(10) Ross J et al. Separation of murine cellular and murine leukemia virus DNA polymerases. Nature New Biology 1971; 231: 163-167.
(11) Beljanski M. Synthèse in vitro de l’ADN sur une matrice d’ARN par une transcriptase d’Esscherichia coli. Comptes rendus de l’Académie des sciences 1972; 274: 2801-2804.
(12) Varmus H. Reverse transcription. Scientific American 1987; 257: 48-54.
(13) Franchi F. In search of HIV; frah08.htm
(14) Strandstrom HV et al. Studies with canine sera that contain antibodies which recognize human immunodeficiency virus structural proteins. Cancer Research 1990; 50: 5628s-5630s.
(15) Papadopulos-Eleopulos E et al. Is a positive Western blot proof of HIV infection? Bio/Technology 1993; 11: 696-707.
(16) Urnovitz HB et al. RNAs in the sera of Persian Gulf War veterans have segments homologous to chromosome 22Q11.2. Clinical and diagnostic laboratory immunology 1999; 6/3: 330-335. See also
(17) Löwer R et al. The viruses in all of us : characteristics and biological significance of human endogenous retrovirus sequences. Proceedings of the National Academy of Sciences USA 1996; 93: 5177-5184.
(18 ) Mullis K. “ Dancing naked in the Mine Field”. Pantheon, 1998.
(19) Gelderblom HR. HIV sequence data base : fine structure of HIV and SIV.
(20) Tahi D. Did Montagnier discover HIV ? “I repeat, we did not purify!”. Continuum 1997; 5: 30-34.
(21) Dourmashkin RR et al. The presence of budding virus-like particles in human lymphoid cells used for HIV cultivation. VIIth International Conference on AIDS. Firenze 1992: 122.
(22) Panem S. C-type virus expression in the placenta. Current Topics in Pathology 1979; 66: 175-189.
(23) Shenton J. “Positively False”. I.B. Tauris & Co, 1998.
(24) Hodgkinson N. “The Failure of Contemporary Science – How a Virus that Never Was Deceived the World”. Fourth Estate, 1996.
(25) Russeil R. “Enquête sur le Sida – Les Vérités Muselées”. Editions Vivez Soleil (Chêne-Bourg/Genève), 1996.
(26) Johnson C. Whose antibodies are they anyway ? Continuum Sept/Oct. 1996.
(27) Weiss R, Wain-Hobson S. The Durban declaration. Nature 2000; 406: 15-16.
(28 ) Stewart GT et al. Not all accepted the Durban Declaration. Nature 2000; 407: 286.
(29) Duesberg P, Köhnlein C, Rasnick D. The chemical bases of the various AIDS epidemics: recreational drugs, anti-viral chemotherapy and malnutrition. Journal of Bioscience 2003, 28 #4: 383-412. See French translation at
(30) Papadopulos-Eleopulos E. A brief history of retroviruses. Continuum 1997; 5: 25-29.
(31) Lanka S. HIV, reality or artefact? Continuum 1995; 3 #1: 4-9.
(32) Rasnick D. The AIDS Blunder. Mail & Guardian (Johannesburg, South Africa), 24 January 2001.
(33) Duesberg P. “Inventing the AIDS Virus”. Regnery, 1996.


  1. Simon said

    I have one question that I’m wondering about.

    De Harven did the following procedure on mouse blood:

    1. Extract plasma
    2. Centrifuge into sucrose gradient
    3. Examine what bands at the 1.16 with an electron micrograph

    And he was rewarded with an excellent view of the Friend retrovirus with very little contamination by non-Friend-retrovirus particles.

    However, when “HIV” researchers have attempted the same steps with blood from “HIV positive” patients, they were cursed with a soup of impure junk banding at 1.16.

    Why is there a such difference between the two since the procedure is basically the same? I suppose my question is, why did De Harven NOT also receive a soup of impure junk in his own experiment? Is it perhaps because in the former case, the ratio of retroviral particles to “everything else which bands at 1.16” is so high, whereas, in the latter case, you’re only getting the “everything else”?

  2. hhbauer said

    I wish I could help here, Simon, but I just don’t know. I don’t know whether ultrafiltration is typically used by HIV researchers before ultracentrifuging, as de Harven says he did.

    Why not e-mail him, he gave his e-address on the article. And please let this blog know if you get a useful response!

  3. Cyril Sader said

    I sent Dr. Etienne De Harven an email with Simon’s question. Below is his response:

    And thank you for a pertinent question !
    I am very pleased that Henry Bauer put my 2003 “Problems with isolating HIV” on his blog;
    but where did you get that I used sucrose gradient to purify the Friend virus?
    I never did!
    I used only a purification method that I had developed, in 1963, at Sloan Kettering in Dr. Charlotte Friend’s laboratory and that included:
    1) collecting the plasma from leukemic mice; 2) filter it through Millipore membrane (0.65 micron pore diameter); 3) filter that first filtrate through another Millipore of smaller pore size, 0.22; 4) ultracentrifuge that second filtrate at high speed (30,000 g) for 2 hours; 5) chemical fixation of the resulting very small pellet and prepare it by plastic embedding for transmission electron microscopy.
    That’s all. There is strictly no sucrose-gradient methodology in my work on Friend virus.
    My method should be described as a double ultrafiltration method.
    It is simple and inexpensive.

    In 2000, Mike Verney-Elliott from London did offer a sizable reward to anybody who would apply my method to the blood plasma of supposedly high-viral-load patients. Nobody ever claimed the award!!
    As you nicely said, if you try that with human blood, all you get is “a soup of impure junk”!!
    Why ?
    Simply because, in my judgement, HIV does not exist!

    I should add that when the sucrose-gradient method was applied, in many other laboratories, to the blood of leukemic mice or birds, it gave good purification of retroviruses (although I didn’t think that it was as nice as mine in level of purity and in level of good preservation of viral ultrastructure!)

    Right: much cell debris does sediment in sucrose at the mystical 1.16 density !!!

    Hope that this is answering your question?
    Best regards,

  4. Andy said

    Great to have Dr. de Harven’s thorough response. In my opinion, Simon’s question remains: Why does de Harven not receive a “soup of impure junk” and at the same time expects receiving such from high “HI-viral load”-patients. I suppose because, as Simon suggests, the ratio of retroviral particles to “everything else at that density” is high when isolating the Friend leukemia virus and low when attempting to isolate “HIV” which, most probably, does not exist.


    Again, would the AIDS-establishment at that point not argue, that although HIV quantity (and therefore ratio) is very low even with high viral load, HIV is such a mysterious, deadly virus that it is able to knock out the immune system even in these extremely low concentrations? Or, differently asked, what IS the establishment responding to this issue?

    Each time trying to give the HIV-AIDS-proponents some chance to justify their claims, they just do not seem to have any explanations for their fallacies.

    What’s most shocking to me is that I have not found a single control experiment (with which I mean a procedure of isolation) which is successful when applied to AIDS patients and fails when applied to healthy people. Is there any such experiment?

    It’d be great to have some opinions on this.

  5. hhbauer said

    I think de Harven’s point (in part) is that his technique of ultrafiltration, which gave the high purification, has not been attempted with HIV.

    Yes: a major problem is that the mainstream refuses to debate the scientific issues.

  6. Zachary said

    My question re: where to find an HIV kit that has been completely isolated thru centrifugation. For some reason my superiors believe Cambridge Bioscience to have developed this pure HIV to be tested sometime in the early 80s but we cannot be certain. Obviously I am in agreement with you–all past HIV research is confounded because isolated HIV is not a hallmark of HIV/AIDS research. If you know what I am talking about it would be most important if you shared the information with me. Thank you.

  7. hhbauer said

    Zachary, I wish I could help, but I know nothing about this

  8. non-believer_of HIV said

    To answer the question, “Why has de Harven’s technique of ultrafiltration has not been attempted?”, is simple. AIDs research generates billions of dollars each year. Without it, these so-called “scientists” (Dr. de Harven and his associates excluded) would be out of a job in short order. If they have been unable to isolate HIV over the past 25 years using their current crude methods, why would they even attempt to use de Harven’s process? The answer is quite elementary… it would destroy their billion-dollar-plus cash cow which they have been feeding off for years (again, Dr. de Harven and his associates excluded). HIV, according to Dr. de Harven, simply does not exist; it’s a myth used to generate funding to research a retrovirus that simply does not exist. Without HIV, the retrovirus that supposedly progresses to AIDS, there is no AIDS research. Why? Because chemo drugs such as AZT would not be prescribed to treat a virus that does not exist. Thus (for me), it is reasonable to conclude that HIV simply does not now, nor has ever, existed, thus *does not* and *cannot* progress to AIDS plain and simple. Chemo AZT treatment and various other antiretroviral treatements are what lead to AIDS. Case in point: Dearly departed Mr. Freddie Mercury. He started recieving AZT treatments once diagnosed as HIV positive and until shortly before his death. So what, exactly, destroyed his immune system? AZT killed his immune system, not HIV, AIDS or any other ARC. End of argument. Ask Dr. Gelderblom what are his thoughts?

  9. Zachary, what is recorded in the Dingell Congressional Commission staff report is that Robert Gallo sent off the ‘HIV” proteins to be used to manufacture the HIV test in early 1994, before Popovic carried out the key experiment that is now widely credited as finding HIV, thus before Gallo could possibly know what proteins were from HIV. It seems what he sent was an untested sample from the material sent to him by the Institut Pasteur (IP).

    I think he sent it to Abbot Labs — as, if I remember right, they were commissioned to make the first HIV tests. The same material was then used to develop PCR probes.

    However, Gallo had many discussions with Cambridge Bioscience — and I think they had a right to his materials — but this needs to be verified. If they did, it was probably the same IP sample that Gallo sent to Abbot. Or was it to Cambridge Bioscience that he sent it first — and they passed it on to Abbot?

    I have other questions to ask about ultra-filtration and HIV. HIV is said to be very delicate — how then could it survive intact after hours of spinning at 30,000 gravities? No human could survive this. Also, could such high-speed spinning force soft particles into a distorted and uniform shape?

    With every good wish,
    author, Fear of the Invisible.

  10. Henry Bauer said

    Zachary, Janine:

    John Crewdson’s Science Fictions is extremely detailed and well documented about what went on in Gallo’s lab

  11. sadunkal said

    Janine Roberts Says:
    “…in early 1994, before Popovic carried out the key experiment…”

    The correct year is 1984 I guess…

  12. Henry Bauer said


    Thanks, I overlooked that. Macdonald too had pointed it out

  13. 1984 of course, that was a typing slip.

    I am sorry to say that Crewdson was not so good in his analysis. I went over the documents he unearthed from Gallo’s lab and found much he had not commented on. Crewdson focussed on proving that it was the French virus LAV that Gallo and Popovic had used in the key experiments – and did not report, although he had the documents in front of him, that Popovic had concluded that he could not prove any virus the cause of AIDS – and that Popovic made no effort to so do. (Gallo had changed the paper at the last moment to hide Popovic’s conclusion.) Also not reported was a letter dated 4 days before the Science papers went for publication from the Head of Electron Microscopy at the NCI to say that the sample Gallo had sent him of the suspected AIDS virus for imaging for publication contained no viruses at all, only cellular debris . Copies of these papers are in the appendix to my book.

    But may I also return to the point that Gallo sent off the materials for the manufacturing of the HIV test before the key experiments were done. This is scientifically an impossible thing to do and robs his patent of all credibility. Crewdson also missed this.


  14. sadunkal said

    I was wondering if there are any recent developments about legal action regarding the 4 papers, all that stuff Gary Null talked about… Were you contacted by any journalist?

    Actually I think all that stuff deserves a long blog post in rethinker blogs, and much more than that… If any reader doesn’t know what I’m talking about, you can find the relevant links if you click on my username.

  15. Marcel said

    Great sleuthing, Janine. Now if only we could find a way to make more than just we dozen or so know about this…

    I agree with Sadunkel that this merits big coverage.

  16. Marcel said

    I’d like to suggest to Janine that Crewdson “missed” these things, probably because he wanted to miss them. His expose morphed into a “limited hangout” exercise when political and economic forces working behind the scenes arranged to sanitize his most explosive findings. Just my opinion, of course.

  17. Marcel said

    This quote from Eleni Eleopulos dovetails nicely with Janine’s findings about Gallo, don’t you think?

    “Gallo claims he had a serum from rabbits that contained antibodies specific to HIV. Just imagine for a moment the scene in Gallo’s laboratory. They’ve cultured H9 cells with lymphocytes from AIDS patients and when they come to determine which proteins in their cultures originate from a presumed virus they reach up on the shelf and, lo and behold, they pull down a bottle labeled ‘specific antibodies to HIV.’ How did they manage to get those antibodies? This was the first paper they wrote but they already had a bottle containing rabbit antibodies specific to a virus they were currently attempting to isolate for the very first time…

    “They say they prepared rabbit antibodies by repeatedly infecting rabbits with HIV. But if they were preparing antibodies to HIV they would have had to inject rabbits with pure HIV which again means they must have already isolated what they were now attempting to do for the first time. It doesn’t make sense.”

    Continuum Autumn 1997


  18. Taras Manolov said

    Dear Henry,

    I looked up the article of Barré-Sinoussi F. et al (that Dr. de Harven cites by #7) and I found e.g. that “periferal blood lymfocites cultured in the same way were consistently negative for the reverse transcriptase activity, even after 6 weeks”. “Same way” here means the same conditions that resulted in propagation of HIV (or T-lymhotropic retrovirus as it is called there) and, according to de Harven, the same conditions that may possibly intiate endogenous retroviruses to “reappear”. To me it seems a sufficiently sound control experiment ruling out endogenous nature of HIV, or at least the virus in question in the Barré-Sinoussis article.

    It appears that Dr. de Harven made some statements that at least in part are not grounded in reality (“Not done were the essential verification experiments that could have clarified the endogenous origin of these viruses”). Would you encourage me to continue taking apart his address? It is kind of embarassing to uncover that such loud and challenging critique of supposed shortcomings of others is based on obviously non-read literature..

  19. Henry Bauer said


    You should query De Harven direct. I have no expertise in these areas, and can go no further than the overall fact that no infectious authentic particles of “HIV” have ever been isolated direct from a supposedly infected person. The burden of proof is on those who claim HV exists in infected people, to prove that it actually does, by demonstrating its presence. They haven’t done it.

  20. Macdonald said

    Dear Taras,

    There may very well be inaccuracies in Prof. DeHarven’s paper, but you haven’t demonstrated any. What you have demonstrated is an astounding ability to miss essential words when you read a simple text.

    The controls Prof. DeHarven is referring to are not tests for RT activity but the EM, which he rightly or wrongly considers essential:

    “In short, it seems that electron microscopy was not used when it was essential to demonstrate the absence of contaminating cell debris in allegedly purified virus preparations, and misinterpreted when stimulated cord blood lymphocytes showed budding retroviruses”

    The RT tests in themselves merely show that no RT activity was observed in one culture, whereas it was observed in another. They say nothing about the source of or reason for the activity. That’s why you need purification and reliable EM.

  21. AltMed said

    It’s all very interesting, and my questions is, why all people, who are not undergoing AZT and other chem-treatments, allegedly having HIV, sooner or later exhibit decrease in T-lymphocytes and decrease in CD4-Helper Cells and consequent ensuing of AIDS. But the people who do not exhibit any ‘antibodies’ to HIV do not have this CD4 decrease in Helper Cells. I am very confused.

    • Henry Bauer said

      Your basic fact is wrong. “HIV+” people DO NOT all “sooner or later exhibit decrease in T-lymphocytes and decrease in CD4-Helper Cells and consequent ensuing of AIDS”. There are many groups of people around the world (Alive & Well, HEAL, informal support groups) who are “HIV+”, healthy, and avoiding all antiretrovirals. To officialdom, some thousands are known under the guise of “elite controllers” or “long-term non-progressors”. Because of the hegemony of HIV/AIDS dogma, there are no reliable statistics about the actual numbers, but they are likely to be large — for example, the CDC has continually estimated that about 1/4 of “HIV+” people don’t know their status, obviously because they’ve never been ill, and that propportion in the United States represents about 1/4 million people.

      • Luwam said

        Dear Henry,
        I have the same question as AltMed. HIV patients that DO have a low CD4 (around 150 or less), or do show a drop in CD4 count, with no co-morbidity, absolutely healthy, ages 20-30. Why do they show a drop in CD4? I’m talking about hiv+ with no ARV treatment, ever.

        Thank you in advance

      • Henry Bauer said

        Luwam: What do CD4 counts in peripheral blood mean?

        (Nothing, according to Dr Juliane Sacher. They vary enormously over time (short! hours!), since they are sent to places where actually needed. )

        What studies have been done on CD4 counts in conditions other than “HIV+”?

  22. lahuesera said


    You are also ignoring, among other things, sufferers of Idiopathic CD4-T-lymphocytopenia. These are people, acknowledged by the medical establishment, as having low CD4 counts and opportunistic infections, but who test negative for HIV antibodies. The numbers of known patients is small and there are few studies and little funding for this phenomenon, which was classified after 1992, when the number of HIV-negative people who exhibited AIDS symptoms were brought to the attention of AIDS specialists by members of the press. There could be many more, who either presented prior to 1992, or who, like most people who test negative, in spite of exhibiting some immune issues, skip off into the sunlight relieved that they “don’t have AIDS.” But, some of those patients who have been studied are very ill indeed, and I’ve seen reference to at least one death, in my reading.

    I am also given to understand, and I am assuredly no expert, that CD4 counts fluctuate in most people and can drop very low in perfectly healthy people.

  23. RaiulBaztepo said

    Very Interesting post! Thank you for such interesting resource!
    PS: Sorry for my bad English, I’v just started to learn this language 😉
    See you!
    Your, Raiul Baztepo

  24. Michael said

    The other quite obvious fact that Altmed is ignoring about CD4 T-cell counts is that the ONLY group of people who ever have their CD4 T-cell count regularly counted, followed, or even observed, are only those who have been diagnosed as HIV-positive.

    Years ago, when CD4 count was FIRST used to declare someone as having AIDS, any count below 500 CD4 T-cells was considered as AIDS. Eventually, it was noticed that many HIV-negative people, including doctors and researchers themselves, found that their own T-cell count could be as low as 250. As the top dogs in HIV research were made aware of this embarrassing fact, the count at which someone was now declared as having AIDS due to a low CD4 T-cell count was lowered to 200.

    Also ignored by Altmed is the fact that, with anyone who is HIV-negative and is found to have a low T-cell count, this low CD4 T-cell count is ignored and the HIV-negative individual with a low count is not even considered to be immune suppressed, at least not unless they happen to test HIV-positive.

    Sometimes, though rare, these CD4 or CD4/CD8 ratio tests may be used to help diagnose or monitor other conditions such as lymphoma, organ transplantation, or DiGeorge syndrome.

    The CD4 count does not even reflect how someone diagnosed with HIV feels or functions. For example, people with higher counts are often ill and have frequent complications, and people with lower CD4 counts quite often have few medical complications and function well.

    Many HIV researchers and clinicians have often noted and even complained that usage of the markers of viral load and CD4 counts appears in the real world to usually be meaningless and makes no sense as to what they actually see with their patients.

    A rational individual would then say “if the tests don’t actually predict anything, then why use them at all”, but without the consensus usage of viral load and CD4 counts, then they would have absolutely nothing at all to use to base diagnoses or drug recommendations on.

    At this point, the rational individual simply points to this fact and declares the HIV researchers and clinicians to simply be irrational.

    At which point the researchers and clinicians get frustrated, and begin to throw their shoes at the rational individual and label him/her a nutty denialist.

    So here we dissidents are yet today, of course believing ourselves to likely be the more rational ones, and continuing to point out to all who have ears to hear and eyes to read that use of both CD4 and viral load counts is, to us, simply irrational.

    And to point out again and for the umpteenth time, that the only reason for continuing to use them is that otherwise “HIV experts” would have nothing to base their divinations and diagnoses and drug recommendations on at all. And we also note that if they gave up using viral load and CD4 counts to prophecy, divine, diagnose, or make drug recommendations to those testing positive, then at that point the only thing they would be able to use to diagnose or drug their HIV-positive patients with would likely be by examination of current cloud patterns, humidity levels, and future weather forecasts.

    And strangely enough, quite possibly, if the “experts” did switch to using the clouds, humidity, and weather forecasts, instead of CD4 and viral load counts, I think that they might actually be more accurate at predicting future illness or health than the CD4 counts and viral load tests, so, at least speaking for myself, I fully encourage this switch.

    • Henry Bauer said

      and the mainstream literature agrees with you. The NIH Treatment Guidelines speak separately about immunologic and virologic failure and clinical progression: meaning that CD4 counts, viral load, and patient health do not change in harmony with one another. The Rodriguez paper showed that viral load doesn’t predict CD4 outcomes.

  25. BradS said

    Does anyone who surfs these waves know anything about the history of FIV (feline Im. virus)? It has an oddly parallel history to HIV. The etiology and symptoms seem to be very similar. I wonder if it has been isolated/purified.

  26. Michael said

    Yes, Brad, FIV and HIV have much in common. And it is more odd and more parallel than you know.

    And the history of the invention of AIDS traces its roots back to FLV and Max Essex. Dr. Jeffery Dach has some of this wonderfully documented and exposed on the dissident site, “You Bet Your Life”. Max Essex himself is the one who originally put it into Gallo’s ear that a retrovirus must be the cause of gay men’s illnesses:

  27. Michael said

    And one more thing, Brad. FIV has more in common with HIV than you think. Just as there are a large number of AIDS dissidents, many cat owners have found that their cats, who were diagnosed as having FIV and were recommended to be euthanized, lived a long healthy life in spite of the FIV diagnosis — FIV: Catching a Bad Case of Rumors.

    Same etiology and symptoms? Or is it the same bad science?

    Strange how one can also most often trace supposed cat AIDS to many other factors such as starvation in feral cats, cats who were exposed to toxins, cats who were weaned before their immune system developed, etc.

    So what are the FIV or HIV tests finding? Who knows! Obviously not the researchers who have been running this supposedly deadly lentivirus scam for the last 25 years.

    It would seem that researchers went quite overboard on the lentivirus theory, soon coming up with cat immunodeficiency viruses, pig immunodeficiency viruses, cattle immunodeficiency viruses, etc., etc., ad nauseum.

    And of course, actual sick animals said to be suffering from pig AIDS, cattle AIDS, etc., also consistently have other stress factors and explanations for any observed actual immune suppression and subsequent illness. They even discovered SIV, and claim it as the cause of illness in monkeys, but the infected wild monkeys do not sicken or die from it. And of course, just finding nondirect evidences presumed to be due to the supposed retroviruses also does not assure any illness in the vast majority of animals testing as positive on any of these indirect tests, just as with humans diagnosed with HIV.

    In all of these animal AIDS cases, just as with HIV, they did not isolate by any classical and proven means, but instead relied on new biotech methods. Nor do they have the EM’s [electron micrographs] of their isolates, nor did they prove transmission, nor did they prove causation. And all we are left with is assumption after assumption based on indirect means of testing and isolation (such as finding RT [reverse transcriptase] activity or using nonspecific antibody tests for antibodies presumed to be caused by the suspected retrovirus), identical to the situation with supposed and presumed to be caused by HIV, human AIDScases.

    With all of the AIDS hype and mass paranoia surrounding it, they may have fooled a lot of people, but fortunately, not everybody bought into their dogma. There are too many other more obvious explanations for nearly all immune suppression in humans and animals. This is why you hear very very little about any of the so-called animal AIDS epidemics anymore.

    Attempting to package it all into a one-size-fits-all or even into a one-size-fits-most retroviral theory of contagious illness has completely failed to live up to any reality in both animals and humans, though it has sure kept a lot of scientists busy and made lots and lots of research funds available to the overzealous reality re-engineers and drug and biotech companies involved.

  28. Marcel said

    I thought it was on the BMJ Debate, but can’t seem to find it now, maybe because I think only part of the BMJ debate is still online. Possibly it was some other web forum. But I remember a few years ago I posted a question to Brian Foley, or maybe it was Nick Bennett, about FIV, as I was also wondering why all of these immunodeficiency viruses for different animals were suddenly appearing in the world, which seemed a pharma marketing department’s dream, and was anticipating the arrival of even more, like PIV (penguin immunodeficiency virus, which would have given the crisis-mongers a useful double Arctic crisis along with the ice caps supposedly melting, the better to obtain lavish funding).

    I am sure that Foley (or Bennett) replied, “FIV doesn’t cause any immune deficiency that I’m aware of.” To which I followed up, “Then why did they name it Feline Immunodeficiency Virus?” along with some sarcastic remarks to which I received no reply that I can recall.

  29. Ronnie said

    So what exactly is HIV doing in the host cell or patients body?

    • Henry Bauer said

      Who says HIV is in any host cell or any patient’s body? Since it has never been extracted from there, how could anyone say that it’s there?

      • Everett said


        We know it is there because of a simple and inexpensive molecular technique called Polymerase Chain Reaction.

        Basically, this technique tells you whether certain fragment of DNA of interest exist in your cell (In this case, HIV’s DNA after it is reverse-trascribed and integrated into the host genome). You simply can not detect presence of HIV’s DNA in the host’s cell.

    • Everett said

      HIV like any other virus has an objective. It has no intention of killing the host, but to use the host as a replicating machinery. The virus keeps replicating and budding out of the host’s cell until the host’s cell burst open; thus, unintentionally kill the host’s cell. Each virus has a specific target cell that it can infect due to the specific “key” it has to “unlock” certain cell. HIV has the key to an important cell in your systemic immune system, therefore it’s bad because it eventually weakens your immunity.

      • Henry Bauer said

        Evidently you have not read the authoritative tome by Jay Levy which admits that it is not understood how HIV does what it’s supposed to do: “None so blind as those who WILL not see”, 2011/06/26

      • Guy said

        Is this true for retrviruses? It was my impression that an important reason Duesberg doubts that a retrovirus could be killing T-cells is that retroviruses don’t kill their hosts. This is why they were once considered a possible cause of cancer: cancer cells don’t die off.

      • Henry Bauer said

        I’ve asked De Harven to respond.

      • Henry Bauer said

        Here’s de Harven’s response:
        ” the name retroviruses was given (I guess around 1976 ???) to RNA viruses that were known before (since around 1958…) as RNA tumor viruses. But they are strictly the same! What was known about RNA tumor viruses automatically applies to “Retroviruses”.
        And RNA tumor viruses were considered (probably since the early 1960) as NON-CYTOLYTIC, meaning that they do not kill the cells they apparently infect. The prototype of these viruses is the Rous sarcoma virus (RSV) on which Peter D. did most of his work in the seventies. I published (probably around 1960 ?) EM pictures of cells undergoing mitotic division AND budding viruses on its surface, and stressed the fact that, obviously, infected cells are alive and well since they divide by mitosis ! In the early days of viral classification, two groups of viruses were frequently identified: the cytolytic and the non-cytolytic viruses, only the viruses of the first group killing the cells they infect, while the viruses of the second don’t. Herpes is a good example of a cytolytic virus, while retroviruses obviously are not cytolytic. Duesberg has always insisted on the fact that if retroviruses cause cancer they most likely enhance cell division, and could not at the same time be cell killers !! This fits well with my early EM pictures showing cells infected with retroviruses while undergoing mitotic division!”

      • Everett said

        Yes you are right, and this is where it gets confusing. In HIV patient, only 1 T cell in 100,000 T cells actually infected by HIV. This, by itself in no way will cause the collapse of one’s immune system. HIV DOES NOT kill the T cell. HOWEVER, The T cells that are infected with HIV kill other T cells in the host.

        Every cell in one’s body has a self-destruct program sequence (you can read more about this topic: apoptosis). In order to activate this program in a cell, a highly specific “key” needs to be inserted in to a highly specific “lock”. Immune cell happens to have a lot of these “key” on the cell surface to kill cells that are infected by pathogens (any kind of pathogens not just HIV) or cells that makes mistake during its lifetime. Immune cells such as T cell, not only has a lot of the “key”, they also have the “lock” as a safety mechanism in case something goes wrong with the T cell itself (such as when it gets infected by virus). When HIV infect a T cell, its mission is to replicate (again, not to kill the host); the T cell which gets infected will try to signal to other immune cell that it was infected and needs to be destroyed. One can obviously see that this will do HIV no good if the current host cell die. So HIV has done the impossible, it forces the current host cell to produce A LOT of “key” localize on the surface of the host cell. What it effectively does is that when other Immune cells try to kill the infected immune cell, they will go through the self-destruct program just by coming in contact with the infected cell (When there are too many “key” on the surface, one will certainly open the “lock” when cells come in contact). This happens in cascade, the more T cells get infected, the more T cells will die. What amazing about HIV is that it use the defense mechanism (self-destruct program) of the host to its advantages.

      • Everett said

        OOPS, to fix what I have said earlier “HIV does not kill the T cell”, change it to “HIV kill T cell, but it’s not the culprit to cause one’s immune system to collapse”

      • Henry Bauer said

        There is no mainstream consensus over how HIV is supposed to cause damage to the immune system.
        Your OOPS and the OOPSed post contradict one another. If HIV kills the cells it infects, then those cells can’t kill other T-cells.

  30. Everett said

    Guy: To answer your question about cancer cell.

    Cancer cell, LIKE HIV infected cell has to evade the programmed Cell Death (PCD) process. This is fairly complicated cell biology but I will try my best to explain. When a living cell possesses a mechanism A, it has to possess another mechanism B to undo/prevent the effect/action of mechanism A. This is falsesafe mechanism used in all living cells. This means, when a cell has forgotten who it was, it becomes cancerous and immortal. Like HIV’s, The cancer cell’s mission is NOT to kill the organism. Its mission is to REPLICATE. As you can see, trying to multiply oneself is the main driving force of evolution and biological processes.

    In order for an organism to live healthfully, billions of cells in one’s body needs to work together independently (yes… together independently). Sometime, a cell needs to sacrifice for the good of the community of cells that forms the organism. Cancer cell refuses to die by doing a lot of things. Firstly, it increase the amount of “Key” (mentioned earlier) on the cell surface so immune cell can not get to it. Secondly, it also increase production of the “seals” to disrupt self-destruct program.

    All in all, infected T cell exhibit some characteristics of cancerous cell (refuse to die). This is probably why some earlier researchers thought it was possible cause of cancer. However, T cell is not immortal and is forced to do this by HIV.

    A lot of other pathogens, however does cause cancer. Those such as HPV, etc…

    • Henry Bauer said

      What you write about cancer cells is what’s called a “just-so story”: nice story, no evidential backing.
      HPV has not been proven to cause cancer. All that’s been found is that a few of the many strains of HPV are quite often associated with cervical cancer. Such correlations NEVER prove causation.

    • Henry Bauer said

      Everett and those who have responded to him:
      (Everett sent another two long comments with links he dug up on Google)
      I e-mailed “Everett” direct as follows:
      Enough already.
      It’s easy to Google and pick up all sorts of stuff. The fact is that there is no agreed mechanism by which HIV is supposed to kill the immune system; see

  31. JustSaying said

    Everett, LOL, your words . . . demonstrate [only] . . . a superficial knowledge of biology and the immune system in general, and mix this . . . with mainstream media nonsense. . . . Please provide references to this increase in “Key” on T-cell surface and then references that indicate this increase actually attracts other T-cells? You say that “HIV” does not kill T-cells directly but when other T-cells link with the infected cell. Funny, your “theory” collides with mainstream media “Theory” of T-cell death in that supposed HIV Experts claim T-cells are killed by viral budding. BTW, please tell me how a virus with 8-11 genes can tell any other cell or any other thing for that matter what to do? This is the continuation of this idiocy that has “HIV” doing everything . . . . The virus that does all things to all people! . . . . Sounds like some 1950s scifi movie . . . .
    [toned down by moderator]

  32. arthur said

    Henry, what do you think of Karri’s death. It made me very sad. I thought she was a decent human being. What do you think when someone like Karri dies? Does it make you question if what we think is correct? you can respond privately using my email.

    • Henry Bauer said

      This is a very important issue and certainly warrants general discussion.
      I think it would be natural for Rethinkers to wonder whether “HIV+” really may be a health threat, when someone like Karri or Christine Maggiore or any other person who tested HIV+ at least once gets ill and later dies. It’s natural for Rethinkers because on the whole we are skeptical people who arrived at our views through looking at evidence, and some of us took a long time before coming to the conclusion that the mainstream is wrong. So we tend to question and doubt, even our own convictions.
      One pitfall is the fact that “HIV+” does indeed seem to be sometimes a marker of some sort of health threat, since the tendency to test “HIV+” increases in populations whose average state of fitness is lower. Recall the data collated in Figure 22 of my book:


      An almost insuperable difficulty is that the full medical records and details of last illness and cause of death are rarely available. When someone dies of heart failure, for example, can one ascribe that to “HIV” or to the fact that the deceased was on antiretroviral drugs for several years in the past? The damage done by those drugs doesn’t necessarily correct itself over time; mitochondrial damage is irreversible, for example.
      It’s also the case that Kalichman and his ilk crow loudly and publicly whenever an “HIV+” Rethinker who refused ARVs later dies, and it’s difficult for Skeptics to break their habit of questioning everything when that happens.
      The best solution, I think, is to keep reminding ourselves of what the data show indisputably:
      — “HIV” is not correlated with “AIDS” (data in my book: no correlation geographically, or chronologically, or in differential effects on men and women, or in differential effects on those of recent African and non-African ancestry).
      — “HIV” tests do not demonstrate infection by “HIV” (Stanley H. Weiss & Elliot P. Cowan, “Laboratory detection of human retroviral infection”, chapter 8 in Gary P. Wormser (ed.). AIDS and Other Manifestations of HIV Infection. London etc.: Academic Press; 2004, 4th ed.)
      — One of the original iconic “AIDS” illnesses, Kaposi’s sarcoma, is indisputably not caused by “HIV”
      — There are so many HIV-negative “AIDS” cases that the mainstream had to invent yet another new disease, idiopathic CD4-T-cell lymphopenia, whose name describes precisely the original AIDS: deficiency of immune-system function in absence of any known cause.
      — Some unknown number of “HIV+” people have remained healthy for more than two decades without antiretroviral treatment. These “long-term non-progressors” or “elite controllers” are a mystery for the mainstream. Calculations indicate that at least half of all “HIV+” individuals are in this category (Galletti & Bauer, “Safety issues in didactic anatomical dissection in regions of high HIV prevalence”, Italian Journal of Anatomy and Epidemiology, 114 [2009] 179-92).
      — The mechanism by which “HIV” is supposed to kill the immune system remains a mystery, as does everything else about HIV: “None so blind as those who WILL not see”, 2011/06/26
      — Other points documented at various times on this blog include that there is no latent period; that the death rate of “people with AIDS” or “HIV+” people does not increase with age; that HAART has not extended lifespan; that people of African ancestry are more prone than others to test “HIV+” and yet they outlive other “HIV+” people.
      It seems incredible and yet it is true, that data from mainstream sources disproves every contention of mainstream HIV/AIDS theory, producing absurdities like the fact that African babies breast-fed exclusively by “HIV+” mothers are less likely to become “HIV+” than babies guarded from their HIV-positive-mothers’ breast milk.

      We will all die, sooner or later, for some reason or other, and the specific reason(s) may not always be evident. Karri Stokely suffered more than a decade of antiretroviral “treatment” and her photographic records show how she became less and less healthy during that time; and the same record shows how she recovered energy and health when she stopped the “treatment”. In my view, the most obvious inference to draw is that her death was brought about by the irreversible part of the damage done by that decade of exposure to ARV drugs.

  33. Henry Bauer said

    Re DC:
    If anyone wants to offer advice, or to get in touch with DC to exchange experiences, I’ll be willing to forward private messages

  34. BSdetector said

    Hello DC,

    First, I would point out the inconsistency in your “numbers”, namely if you will notice that your “viral load” went to 305,000, yet during this same period your t-cells increased. Odd isn’t it that what is supposedly killing your t-cells, when increased, would increase your t-cells during this period?

    As for this “viral load” test, I would totally ignore these numbers. The “test” is useless. Even the package insert for this test states that “it is not to be used for clinical diagnostic purposes, as the test results and their relationship to actual blood viremia has not be shown”. With the terror instilled in you by these bogus tests, the “viral load” could just as easily be measuring some type of stress related product. You are correct in your thought that high stress can have disastrous effects on the immune system. You are also astute in your observation that your t-cell numbers were not measured prior to you becoming “HIV positive” and therefore it is foolhardy to absolutely claim that “low” t-cells now are related to “HIV”. This is one of the biggest problems I have with this test. There has never been any studies that investigate what “normal” t-cell levels are and how major stressors (cancer diagnosis, death in family, divorce, job loss) can have on these levels. Also, there are people, again NO ONE knows how many, who are referred to as having idiopathic lymphocytopenia. in these people, low t-cells are normal and they have always had low t-cells.

    You need to start educating yourself about all the “tests” that are being performed on you, the historical background of HIV, and that the medical profession and its current pimp, the pharmaceutical industry, has many failures to its name. If you look at three of the pharma industry’s biggest profit makers: depression, high cholesterol, and HIV, all three are mostly based on garbage science.

    Knowledge is power. Take control of your health and your health care. DO NOT assume that the medical profession knows everything. Educate yourself and then go into your MD and start asking some difficult and astute questions and you will quickly discover that he/she probably does not know much more than you. Then the question becomes: why are you telling me this condition is 100% fatal and your life-giving drugs will only save me? Be like Toto in the Wizard of Oz. Remember when he pulled the curtain back and revealed the Wizard to be just a lonely old man pulling levers? LOL

    • Henry Bauer said

      Nothing is risked by eating some probiotics which have in some cases increased CD4 counts. I’ve been taking SupremaDophilus without any signs of harm for several years, alternating with Soil-Based Organisms from Swanson. They’re also quite cheap.

  35. BSdetector said

    Hello DC,

    LOL, I am sorry to laugh at your dimwitted doctor’s response that you have an “aggressive” strain of HIV, but that is exactly what an MD told a friend of mine. It is just laughable how these people seem to make BS up as they go along. You might know this, but one of the foundational claims in the HIV=AIDS blather is that the reason why there is a 8-10-year latency period of disease progression is that the virus is a lentivirus, or a slow virus. You might ask your doctor how a “Slow” virus transforms into a “fast” virus? Specifically? Ask him for 3 articles from peer-reviewed scientific journals to substantiate this remarkable transformation. LMAO! What is claimed to be “HIV” has from 8-12 genes. It is absolutely preposterous that such a simple organism could somehow change its behavior, or that any person could have such a response that is completely different than that found in other patients. One possible logical explanation is that HIV infection may be one factor in T-cell reduction, and that patients who present with a rapid T-cell loss also are positive for other factors. But, again, NO MD or researcher has indicated that other factors other than HIV are involved in T-cell loss. So they cannot say this because it would be contrary to their entire dogma.

    Regarding my friend’s case, his T-cells also tested “low” from the very first testing. The MD told him that his infection must be “old”. Unfortunately, my friend had an “HIV antibody test” performed every 1-2 years. This means that either the claim that HIV progresses over a set measurable period is wrong, or the 3-4 antibody tests were in fact false negatives. In either case, their theory suffered greatly. What bothers me most about this medical advice is that here we have an obvious grotesque inconsistency with the established clinical presentation, yet no one bothers to investigate these anomalies. This is NOT science. If I measured the speed of light in New York and then also Los Angeles, but the results I obtained in LA were different than those in New York, does it make any sense at all to report the speed of light as that found in New York and just ignore the results obtained for LA? In real science, you must investigate all results that deviate from your hypothesis. This is especially required if you intend on telling patients that they have a 100% fatal condition!

    • Henry Bauer said

      BSdetector, DC:
      Actually, HIV starts as a normal fast virus, since it’s said to cause “acute” infection immediately, with high viremia, lots of more HIV production during the “window” of some weeks in which it is undetectable by antibody tests. Then it somehow converts into a lentivirus, or hides somewhere, before emerging again and become vicious 10 years later.

  36. angela said

    I am being to believe , I tested poz like 12 thru my mum who ordered , but she didn’t tell me but told my sis . The other day after 12yrs I went and tested myself and my results were poz. My vl was 281000 and CD 4 of 318 . with no illness never admitted my doc started me on ARV immeadiately.explained that my cd4 will increase slowly and virus will take 6months and end up 1500 after six months I went back my cd 4 was 800 and detectable vl with yellow eyes due to cocktail . I asked the same and am wondering does hiv exist since I guess I have just taken a lot of vitamin c and feel great . I tested again and my result came back negative. I have booked an appointment with my doc.. After eight months . My question I should have tested for syphilis . That’s what some one told that when you r positive for syphilis your hiv test will positive

  37. Lucas B. said

    Having a low CD4+ T count in the blood is characteristic of healthy people. Your CD4+ T-cells must be somewhere else (tissues & glands), not in your blood. There’s no HIV viral-load count because first, HIV cannot be isolated and so cannot be counted; and second, because what the viral load is supposed to be are the antibodies, who are not being sufficiently produced since the medication, cocktail or whatsoever HAART is destroying your B cells; B comes from Bone marrow, which is one the few “things” the HAART attacks.

    It’s all a vicious circle that always takes us to STEP 1: Where’s the HIV in “infected” people? “We” are diagnosing and treating an imaginary retrovirus. The talk is useless then. Could HIV exist? Maybe. Is it sexually transmitted? If we follow the “orthodox” tests, no. Is the hypothetical HIV the cause of AIDS? Without a proper isolation and further studies, the question sounds stupid. Does AIDS exist? AIDS is a word. The diseases do exist and may have different causes depending on so many factors, factors who differ from a person to another since 2 humans are never identical, from an environment to another, and so on. But yes, the MAIN factors should be the same.

    So, bottom line, I can’t understand a scientific debate on an unproven and unstudied syndrome, which is supposed to be “mainly” caused by a hypothetical retrovirus, a retrovirus that has not been isolated, but yet its presence in human blood can be tested/verified (?!).

    Reading the last 2 paragraphs, even an extraterrestrial might laugh at how stupid this HIV/AIDS story is. Sadly, it has taken and it is taking so many lives. Humans are their own angels and devils.

    PS. Sorry for my poor English.


  38. Cristian said

    Been almost 3 yrs. Any update on your situation, DC ? Did you do something ?

  39. Ls said

    And how is ur situation at this moment dc ?

  40. The X man said


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