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Unpublished commentary on Gallo RC, Montagnier L. The discovery of HIV as the cause of AIDS. New England Journal of Medicine 2003;349:2283-5.


It is a pity that Robert Gallo and Luc Montagnier1 do not provide readers of the Journal with references to back up their many claims regarding the proof for the existence of HIV and its role in AIDS.  Especially since many of their claim are questionable.  For example:


(1)     "…the causative relationship between HIV and AIDS was accepted by the scientific and medical community…"  Not everybody in the scientific community accepted that they proved the existence of HIV and its causative role in AIDS.2-4 Also, acceptance of a theory does not prove the theory correct.


(2)     "In early 1983, a clear-cut isolate [HIV] was obtained in Paris…".  However, in 1984 Gallo and his colleagues said that Montagnier and his group's 1983 evidence did not prove "true isolation".5  As late as 1997 Jaap Goudsmit wrote: "The BRU lymph node was first cultured in early January 1983 and, on January 15, it shed an enzyme absolutely unique to the lentivirus group…The BRU virus grew slowly and with difficulty, but its identity and activity were reported in the May 20, 1983 issue of Science…The Pasteur Group was widely acclaimed but very worried.  In the world of virology, finding a new virus is not enough:  You must propagate and isolate the organism for analysis by other virologists.  The French had not yet isolated their new lentivirus";6


(3)     "…reverse transcriptase - the enzyme that is present in all retroviruses…".  It is true that this enzyme is present in all retroviruses, including lentiviruses and that the detection of reverse transcription was considered by Montagnier proof for HIV isolation.  But it is also true that the enzyme is not unique to these viruses, much less to lentiviruses.  Furthermore, all the HIV experts including Gallo and Montagnier have proven the presence of the enzyme indirectly, that is, by transcription of the synthetic template-primer An.dT15.  However, even before the AIDS era, at least Gallo and the principal and second authors of the Montagnier 1983 study were aware that this template-primer can be transcribed by cellular DNA polymerases7-9 as was proven by Montagnier himself in 1984.10


(4)     "…the centres for Disease Control and Prevention (CDC) reported cases of AIDS in patients with haemophilia who had received only filtered clotting factors, which seemed to eliminate the possibility that the agent was a micro-organism larger than a virus".  If AIDS is caused by filtered factor VIII it does not mean that the cause is a virus.  The cause could be something even smaller than a virus.  If as Gallo and Montagnier claim at the basis of the clinical manifestations of AIDS is a decrease in T4 cells, then given the fact that Robin Weiss and the CDC have shown that in haemophiliacs, "the abnormal T-lymphocyte subsets are a result of the intravenous infusion of factor VIII concentrates per se, not HTLV-III [HIV] infection"11, 12 then one would have to conclude that the cause of AIDS in haemophiliacs is factor VIII and not HIV.  Furthermore if:  (a) as some of the most eminent HIV experts, including Montagnier claim that:  "gp120 is crucial to HIV's ability to infect new cells", and gp120 is present only in the HIV particles spikes (knobs);13, 14  (b) to date nobody has proven the existence of spikes in the cell-free HIV particles;15 (c) Factor VIII is made from cell-free plasma;  (d) according to the  CDC “drying of HIV-infected human blood or other body fluids reduces the theoretical risk of environmental transmission to that which has been observed--essentially zero";16 (e) Factor VIII is a freeze dried powder several months or even years old before use;  then if the cause of AIDS in haemophiliacs is a virus, the virus would have to be other than HIV.


(5)     "The growth of the putative virus in T-cell lines was an enormous step, facilitating the development of a blood test for HIV, which…produced convincing evidence of the association between HIV infection and AIDS".  To obtain antigens for the development of the blood test (antibody test) one must obtain a large amount of the virus and, as Montagnier points out,17 purify the virus.  In 1997 Montagnier acknowledged that in 1983 his team did not purify the virus, and in his view, neither did Gallo's in 1984.17  Neither has anybody else since.  Even if there is proof beyond reasonable doubt that the antigens in the antibody test are HIV proteins, proof must exist that they do not cross-react with antibodies which are elicited by agents other than HIV.  However, the specificity of the antibody tests has never been proven and, due to the lack of a gold standard, cannot be proven.3  Furthermore, Essex and his colleagues have shown that antibodies to carbohydrate-containing antigens such as lipoarabinomannan, which are present in all mycobacteria and fungi, react with the antigens in the HIV tests.18  Since the vast majority of the opportunistic infections which signify AIDS are caused by mycobacteria or fungi a correlation between a positive antibody test and AIDS may be present in the absence of HIV19, 20  Most importantly, even if an association between HIV and AIDS existed, such an association is not proof for causation.


(6)     "…AIDS had already appeared as a long-lasting disease, with an extremely long time between exposure to the agent (through blood or sexual activity) and the profound state of immune suppression characterised by the occurrence of opportunistic infections or cancers".  If the causative agent of AIDS is sexually transmitted, then the agent cannot be HIV.  The main absolute necessary property of sexually transmitted agents is bidirectionality, that is transmission from the passive to the active partner and vice versa.  To date there is no proof that this is the case for HIV.  In 1984 Gallo and his colleagues reported that "Of eight different sex acts, seropositivity correlated only with receptive anal intercourse…and with manual stimulation of the subject's rectum (receptive "fisting")…and was inversely correlated with insertive anal intercourse".21  Two years later they confirmed their 1984 findings"  "In this analysis, only receptive rectal intercourse, douching, rectal bleeding…were significant predictors (p<.05) of anti-HTLV-III positivity…We found no evidence that other forms of sexual activity contributed to the risk".22  In a 1994 review of all the major studies conducted in gay men the authors concluded:  "(1) unprotected anogenital receptive intercourse poses the highest risk for the sexual acquisition of HIV-1 infection;  (2) anogenital insertive intercourse poses the highest risk for the sexual transmission of HIV-1 infection…(5) no or no consistent risk for the acquisition of HIV-1 infection has been reported regarding other sexual practices such as anogenital insertive intercourse and oroanal sex…"23


          Since only the passive partner becomes seropositive then, at least in gay men, HIV, like pregnancy, can be sexually acquired but not sexually transmitted.  The largest, longest, best designed and executed studies conducted in the USA and Africa show that HIV is not heterosexually transmitted.24-27


Eleni Papadopulos-Eleopulos  Biophysicist, Department of Medical Physics, Royal Perth Hospital, Perth, Western Australia

Valendar F. Turner  Consultant Emergency Physician, Department of Emergency Medicine, Royal Perth Hospital, Perth, Western Australia

John M Papadimitriou  Professor of Pathology, University of Western Australia, Perth, Western Australia

Barry A. P. Page  Physicist, Department of Medical Physics, Royal Perth Hospital, Perth, Western Australia

Helman Alfonso  Lecturer, School of Public Health, Curtin University, Western Australia

David Causer Physicist, Department of Medical Physics, Royal Perth Hospital, Perth, Western Australia

Sam Mhlongo  Head & Chief Family Practitioner, Family Medicine & Primary Health Care, Medical University of South Africa, Pretoria, South Africa

Todd Miller  Research Assistant Professor,  Department of Medicine, Division of

Cardiology, University of Miami School of Medicine, Florida, United States of America

Andrew Maniotis, Department of Pathology, University of Illinois at Chicago, United States of America

Christian Fiala  Specialist in Gynaecology, Vienna, Austria




1.             Gallo RC, Montagnier L. The discovery of HIV as the cause of AIDS. New England Journal of Medicine 2003; 349:2283-5.

2.             Duesberg PH. Retroviruses as carcinogens and pathogens: Expectations and reality. Cancer Research 1987; 47:1199-1220.

3.             Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. Is a positive Western blot proof of HIV infection? Bio/Technology 1993; 11:696-707.

4.             Papadopulos-Eleopulos E. Reappraisal of AIDS: Is the oxidation caused by the risk factors the primary cause? Medical Hypotheses 1988; 25:151-162.

5.             Popovic M, Sarngadharan MG, Read E, Gallo RC. Detection, Isolation,and Continuous Production of Cytopathic Retroviruses (HTLV-III) from Patients with AIDS and Pre-AIDS. Science 1984; 224:497-500.

6.             Goudsmit G. Viral Sex-The Nature of AIDS. New York: Oxford University Press, 1997.

7.             Sinoussi F, Mendiola L, Chermann JC. Purification and partial differentiation of the particles of murine sarcoma virus (M. MSV) according to their sedimentation rates in sucrose density gradients. Spectra 1973; 4:237-243.

8.             Toplin I. Tumor Virus Purification using Zonal Rotors. Spectra 1973:225-235.

9.             Weissbach A, Baltimore D, Bollum F. Nomenclature of eukaryotic DNA polymerases. Science 1975; 190:401-402.

10.           Rey MA, Spire B, Dormont D, Barre-Sinoussi F, Montagnier L, Chermann JC. Characterization of the RNA dependent DNA polymerase of a new human T-lymphotropic retrovirus (lymphadenopathy associated virus). Biochemical and Biophysical Research Communications 1984; 121:126-33.

11.           Jason JJ, McDougal S, Holman RC, et al. Human T-lymphotropic retrovirus type III/lymphadenopathy-associated virus antibody. Journal of the American Medical Association 1985; 253:3409-3415.

12.           Ludlam CA, Steel CM, Cheingsong-Popov R, et al. Human T-Lymphotropic Virus Type-III (HTLV-III) Infection in Seronegative Haemophiliacs after Transfusion of Factor VIII. Lancet 1985; II:233-236.

13.           Haseltine WA, Wong-Staal F. The molecular biology of the AIDS virus. Scientific Medicine 1988; 259:34-42.

14.           Gougeon ML, Laurent-Crawford AG, Hovanessian AG, Montagnier L. Direct and indirect mechanisms mediating apoptosis during HIV infection: contribution to in vivo CD4 T cell depletion. Immunology 1993; 5:187-194.

15.           Layne SP, Merges MJ, Dembo M, et al. Factors underlying spontaneous inactivation and susceptibility to neutralization of human immunodeficiency virus. Virology 1992; 189:695-714.

16.           CDC. Fact sheet on HIV transmission. Fact sheet on HIV transmission 1994; January.

17.           Tahi D. Did Luc Montagnier discover HIV?  Text of video interview with Professor Luc Montagnier at the Pasteur Institute July 18th 1997. Continuum 1998; 5:30-34.

18.           Kashala O, Marlink R, Ilunga M, et al. Infection with human immunodeficiency virus type 1 (HIV-1) and human T cell lymphotropic viruses among leprosy patients and contacts: correlation between HIV-1 cross-reactivity and antibodies to lipoarabinomannan. Journal of Infectious Diseases 1994; 169:296-304.

19.           Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D, Page B. HIV antibody tests and viral load - more unanswered questions and a further plea for clarification. Current Medical Research and Opinion 1998; 14:185-186.

20.           Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D. The Isolation of HIV: Has it  really been achieved? Continuum 1996; 4:1s-24s.

21.           Goedert JJ, Sarngadharan MG, Biggar RJ, et al. Determinants of retrovirus (HTLV-III) antibody and immunodeficiency conditions in homosexual men. Lancet 1984; 2:711-6.

22.           Stevens CE, Taylor PE, Zang EA, et al. Human T-cell lymphotropic virus type III infection in a cohort of homosexual men in New York City. Journal of the American Medical Association 1986; 255:2167-2172.

23.           Caceres CF, van Griensven GJP. Male homosexual transmission of HIV-1. AIDS 1994; 8:1051-1061.

24.           Gray RH, Wawer MJ, Brookmeyer R, et al. Probability of HIV-1 transmission per coital act in monogamous heterosexual, HIV-1 discordant couples in Rakai, Uganda. Lancet 2001; 357:1149-1153.

25.           Kamali A, Quigley M, Nakiyingi J, et al. Syndromic management of sexually-transmitted infections and behaviour change interventions on transmission of HIV-1 in rural Uganda: a community randomised trial. Lancet 2003; 361:645-52.

26.           Padian NS, Shiboski SC, Glass SO, Vittinghoff E. Heterosexual transmission of human immunodeficiency virus (HIV) in northern California: results from a ten-year study. American Journal of Epidemiology 1997; 146:350-357.

27.           Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, et al. Global voices on HIV/AIDS. Heterosexual transmission of HIV in Africa is no higher than anywhere else. British Medical Journal 2002; 324:1035.