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(c) evidence also existed that many factors including infections, and trivial ones, such as exposure to the sun or radiation in solaria lead to decreased T4 cells. Although some of the T4 decreases were long lasting, the patients did not develop KS and OI;4 a significant proportion of the "AIDS" patients, including patients with KS and OI infections, had normal numbers of T4 cells.4 In other words, T4 decrease (immune deficiency) is neither necessary nor sufficient for the development of KS and OI. Thus the proposition that KS and the OI are the result of T4 decrease and that the T4 decrease detected in the patients belonging to the AIDS risk groups was caused by HIV infection was totally inconsistent with the data available even before the hypothesis was put forward. For some time now, all HIV/AIDS experts, including Robert Gallo, accept that HIV has no direct or indirect role in KS.5-7
FAILED PREDICTIONS
The HIV theory predicted that HIV was sexually transmitted and therefore AIDS would spread throughout the heterosexual population. Obviously this has not happened. The prediction by proponents of the HIV theory that a vaccine would be developed by 1986 also has not been fulfilled. In 1984 Montagnier said that the only way to prove HIV is the cause of AIDS is to have an animal model.8 Although no effort has been spared, no model of a retrovirus causing AIDS has been forthcoming. Indeed, the only animal model that bears any resemblance to human AIDS fully supports a non-infectious modus operandi.9
WHAT LED A PHYSICIST TO STUDY AIDS
At the outbreak of AIDS, Gallo had already spent a decade in attempts to prove that the cause of some cancers was a retrovirus. This led him to put forward the retroviral theory of AIDS. From an equally biased position I put my non-infectious theory. Although trained as a nuclear physicist, with the exception of a few years, I have worked in the medical field in the Department of Medical Physics of the Royal Perth Hospital, the largest teaching hospital in Western Australia. Among its many activities it was involved in treating cancer by radiation and pioneered hyperthermia for the same purpose.
It was known that both radiation and radio-sensitisers were oxidising agents, and apart from hyperbaric oxygen the chemical radiosensitiser included compounds containing the -NO2 group, that is, nitro-compounds. To understand the interaction between the agents used to treat cancer and cancer tissue, I first needed to determine what makes a cell cancerous. I decided the best way to approach this was to attempt to fully understand the normal cell. This included the understanding of the mechanism by which sperm induced the division of the ova. In doing so I developed my own theory of biological functioning. A short version was first presented at a meeting in Colorado in 1979 and was published in Speculation in Science and Technology in 1980. A more detailed version was published in 1982 in the Journal of Theoretical Biology, after it was first rejected by Nature, under the title "A Mitotic Theory". Although the title suggests that it deals only with cellular division and cancer, the theory, as one of the reviewers pointed out, also proposed a "relationship between modifications in the redox state of the actin-myosin system and other key biological processes (e.g. transport, muscle function, metabolism...). Most importantly in this article, there is a clear integration of older and present data as well as "classical" and "contemporary" concepts.
The theory claimed that the cellular redox level and its oscillations, that is, the cyclic variation between oxidation and reduction, plays a pivotal role in both normal and abnormal cellular function and structure. Diseases such as cancer, cardiovascular, clotting abnormalities and ageing, for example are the result of perturbation of the cellular redox level and its oscillations.
Thus, by the time AIDS was diagnosed I was aware of the biological and pathological effects induced by many agents (semen, nitrites, recreational drugs, Factor VIII, infectious agents and the drugs used to eradicate them) to which the patients belonging to the AIDS risk groups were exposed.
More importantly all these agents showed a common property: they were oxidising agents. This led me to put forward the non-infectious theory of AIDS which claimed that the primary risk factors for AIDS were the oxidising agents to which the individuals were exposed. While the manuscript discussing this theory (in which neither HTLV-I nor Montagnier's retrovirus were mentioned) was in the hands of a few colleagues for evaluation, Gallo claimed to have proven that HTLV-III was the cause of AIDS. I was advised to re-write the manuscript to take account of these claims. The revised manuscript, which was twice rejected by Nature and initially by Medical Hypotheses, was later accepted by the latter journal.
PREDICTION OF THE OXIDATIVE STRESS THEORY OF AIDS
The predictions of my theory included:
(1) AIDS would remain restricted to the risk groups. This has been the case.
(2) The only sexual act leading to AIDS or a positive antibody test is a very high frequency of receptive anal intercourse in either sex. One of the first to publish supporting evidence of this was Gallo and his associates. In a study published in 1984 he wrote: "of eight different sex acts, seropositivity correlated only with receptive anal intercourse...and was inversely correlated with insertive anal intercourse.10 In 1986 Gallo wrote: "Data from this and previous studies have shown that receptive rectal intercourse, for example, is an important risk factor for HTLV-III [HIV] infection. Yet, at the time of entry into this project, nearly half of the participants still practised this technique. We found no evidence that other forms of sexual activity contributed to the risk".11 Thus Gallo was one of the first to publish evidence which contradicted his own assertion that HIV/AIDS is bi-directionally sexually transmitted.
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(6) Perhaps the boldest claims and predictions were made regarding the existence of HIV. I wrote HIV, "has never been isolated from fresh AIDS tissues". Furthermore, HIV "has never been isolated as an independent stable particle". That is, HIV had not been isolated from either fresh tissues or culture, which means that its existence had not been proven and this situation has not changed up to the present day. At least Montagnier in his 1997 interview to Djamel Tahi admitted that he had not isolated HIV and in his view neither had Gallo,32. I presented evidence that the observed phenomena (particles, reverse transcriptase, antibody/antigen reactions) which were said to prove the existence of HIV were not specific to a specific retrovirus nor even to retroviruses in general. Unlike Gallo, Montagnier when interviewed by Djamel Tahi, eventually reluctantly admitted that these phenomena were not retrovirus specific. I cited examples of evidence which, taken together, led to the conclusion that oxidising agents were causing not only AIDS but also gave rise to the phenomena which were interpreted by the Montagnier and Gallo school as indicating the presence of HIV. As far back as 1986 Montagnier knew that the phenomena could not be obtained unless the cultures were stimulated, although he did not know that the stimulants were oxidising agents,33. In 1991 Anthony Fauci proved that the "HIV" phenomena could be inhibited by antioxidants,34.
CONCLUSION
It is over twenty years since I conceived the redox theory of cellular function and nearly as long since its specific application to the problem of AIDS appeared in Medical Hypotheses. I look back over this time with very mixed feelings. Naturally I am proud that as a scientific theory every prediction concerning AIDS has materialised. However, I am saddened that there are forces at work which have consistently prevented purposeful but friendly debate. To me and my group the problematic nature of the HIV theory was apparent from the very beginning. It is now my fervent hope that, as the HIV theory continues to fail the many patients who are diagnosed with antibodies to "HIV" and AIDS, the time is rapidly approaching when scientists and physicians will be eager to examine our contribution.
REFERENCES
Montagnier L. (1985). Lymphadenopathy-Associated Virus: From Molecular Biology to Pathogenicity. Ann. Int. Med. 103:689-693.
Ludlam CA, Steel CM, Cheingsong-Popov R, et al. (1985). Human T- Lymphotropic Virus Type-III (HTLV-III) Infection in Seronegative Haemophiliacs after Transfusion of Factor VIII. Lancet II:233-236.
Jason JM, McDougal JS, Dixon G, et al. (1986). HTLV-III/LAV Antibody and Immune Status of Household Contacts and Sexual Partners of Persons with Haemophilia. JAMA 255:212-215.
Papadopulos-Eleopoulos E, Turner VF, Papadimitriou JM, Hedland- Thomas B, Causer D, Page B. (1995). A critical analysis of the HIV-T4- cell-AIDS hypothesis. Genetica 95:5-24.
Papadopulos-Eleopulos E. (1988). Reappraisal of AIDS: Is the oxidation caused by the risk factors the primary cause? Med. Hypotheses 25:151-162.
Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. (1992). Kaposi's sarcoma and HIV. Med. Hypotheses 39:22-9.
Lauritsen JL. NIDA meeting calls for research into the poppers-Kaposi's sarcoma connection. (1995). p. 325-330 In: AIDS: Virus- or Drug Induced Duesberg PH, ed Kluwer Academic Publishers, London.
Vilmer E, Rouzioux C, Vezinet Brun F, et al. (1984). Isolation of new lymphotropic retrovirus from two siblings with Haemophilia B, one with AIDS. Lancet I:753-757.
Ter-Grigorov VS, Krifuks O, Liubashevsky E, Nyska A, Trainin Z, Toder V. (1997). A new transmissible AIDS-like disease in mice induced by alloimmune stimuli. Nat. Med. 3:37-41.
Goedert JJ, Sarngadharan MG, Biggar RJ, et al. (1984). Determinants of retrovirus (HTLV-III) antibody and immunodeficiency conditions in homosexual men. Lancet 2:711-6.
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