(ii) At present there is evidence that studies with “negative” findings, that is studies with findings at odds with what is expected, are difficult to publish. “Negative studies suffer a substantial time lag. With some exceptions, most of this lag is generated after a trial has been completed…Typical examples in HIV disease include the use of early zidovudine monotherapy in asymptomatic patients, acyclovir, ditiocarb (Imuthiol), and oral graniclovir prophylaxis, where positive and negative trials started at about the same time, but negative studies appeared later or are still unpublished”.3

It is true “the idea that there is a direct, causal relationship between infection with the human immunodeficiency virus (HIV) and the onset of AIDS”, has survived the peer-review system. However, it is also true that “intellectual scrutiny and testing through experiment” show that:

(1) The HIV hypothesis of AIDS was put forward to account for the high frequency of some clinical and laboratory phenomena in gay men, IV drug users and haemophiliacs, none of which were new. The main clinical phenomena were Kaposi’s sarcoma (KS) and Pneumocystis carinii pneumonia, the former constituting the basis for a relationship between AIDS and retroviruses. At present everybody including the CDC acknowledge that HIV plays no role, either directly or indirectly in the development of KS.4, 5

(2) The laboratory phenomenon was a decrease in T4 cells, determined by the use of antibodies, in blood (Acquired Immune Deficiency). Destruction of the T4 cells by HIV was said to be the “hallmark” of HIV infection.6 However, one year after the acceptance of the HIV theory, Weiss, Ludlam et al wrote (concerning patients with haemophilia): “Our finding…supports our previous conclusion that the abnormal T-lymphocyte subsets are a result of the intravenous infusion of Factor VIII concentrates per se not HTLV-III infection”.7 One year later researchers from CDC claimed, “...factor concentrate (Factor VIII) itself may be immunosuppressive even when produced from a population of donors not at risk of AIDS.8 In 1985 Montagnier wrote: “This syndrome [the AIDS diseases] occurs in a minority of infected persons, who generally have in common a past of antigenic stimulation and of immune depression before LAV [HIV] infection”.9 More importantly, at present there is evidence that the decrease of T4 cells in blood is not due to their destruction by HIV or any other factor. “This article discusses the importance of alterations in the CD4+ and CD8+ cell migration in regulating blood lymphocyte levels and questions the extent of virus-mediated CD4+ cell destruction”,10 “CD4+ T-cell lymphopenia is due to both shortened survival time and a failure to increase the production of circulating CD4+ T-cells”,11 or to the down-regulation of the CD4 molecule.12

(3) It was accepted that no single infectious agent could possibly be the direct cause of the multiple diseases seen in AIDS patients. It was postulated then that the destruction of T4 cells (the immune deficiency) inevitably led to the appearance of KS and the opportunistic infections. At present, evidence exists which proves that T4 decrease is neither necessary nor sufficient for the syndrome to develop. “CD4 [T4] cell counts were not significantly associated with the risk of progression” to disease.13 “Along with other recent analyses and experimental developments these conditions also suggest a need to re-evaluate current concepts about HIV pathogens including the concept that a systemic depletion of CD4 T-cells is the hallmark of the disease”.14

(4) Although as the proponents of the HIV theory predicted many drugs have been developed to treat HIV infection, the beneficial clinical effects of these, if any, cannot be due to their anti-HIV effect. With no exception, all the anti-HIV drugs presently used, by design can only prevent the synthesis of HIV DNA. Once the DNA is formed they cannot prevent the transcription of the DNA into RNA. In other words the drugs can decrease HIV RNA only indirectly, by decreasing the HIV DNA. The presently available data shows that no drug, and no drug combination, including Highly Active Antiretroviral Therapy (HAART) decreases the “viral burden”, that is HIV DNA.1, 15, 16. In fact, HAART can lead to “a significant increase in PBMC proviral DNA”.17

(5) According to the HIV theory of AIDS, haemophiliacs acquire HIV via contaminated factor VIII. Yet CDC data show that this is not possible. Their data shows that HIV “does not spread or maintain infectiousness outside its host. Although these unnatural concentrations of HIV can be kept alive under precisely controlled and limited laboratory conditions, CDC studies have shown that drying of even these high concentrations of HIV reduces the number of infectious viruses by 90 to 99 percent within several hours. Since the HIV concentrations used in laboratory studies are much higher than those actually found in blood or other body specimens, 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".18

(6) The main prediction of the HIV theory of AIDS was, that although AIDS was first diagnosed in gay men, because AIDS was caused by a sexually transmitted agent, which like all other such agents, is bidirectionally transmitted, AIDS, would rapidly spread throughout the heterosexual population. One of the first scientists to publish data that this could not be the case, at least in gay men, was Robert Gallo and his associates. In 1984 he wrote: “Of eight different sex acts, seropositivity correlated only with receptive anal intercourse….”.19 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…We found no evidence that other forms of sexual activity contributed to the risk”.20 This was confirmed in many other studies including the Multicenter AIDS Cohort Study, (MACS) the best, largest (about 5,000 men), and longest study which commenced in 1984 and is ongoing.21 In this, as well as other studies, it was shown that it is the frequency of passive anal passive intercourse, not the number of partners which is important in the development of a positive antibody test and AIDS.22-24 In a 1994 review of most, if not all the epidemiological studies conducted in gay men, the authors concluded: “it can be said that the cited reports yield convincing evidence that (1) unprotected ano-genital receptive intercourse poses the highest risk for the sexual acquisition of HIV-1 infection; (2) ano-genital insertive intercourse poses the highest risk for the sexual transmission of HIV-1 infection; (3) there is mounting epidemiological evidence for a small risk attached to oro-genital receptive sex, biologic plausibility, credible case reports and some studies show a modest risk, detectable only with powerful designs; (4) sexual practices involving the rectum and the presence of (ulcerative) STD facilitate the acquisition of HIV-1; (5) no or no consistent risk for the acquisition of HIV-1 infection has been reported regarding other sexual practices such as ano-genital insertive intercourse and oro-anal sex….(8) the association of substance use with HIV infection is probably the result of interaction, because substance use increases the likelihood of practising ano-genital receptive intercourse”.25 Unquestionably, to date, the best designed and executed study in heterosexuals was conducted by Nancy Padian and her associates. In 1987 they reported: “The total number of exposure to the index case (sexual contacts with ejaculation) and the specific practice of anal intercourse” were associated with the development of a positive antibody test. The results from their long (ten years) prospective study of heterosexual couples of whom only one partner of either sex was antibody positive were published in 1997 where they reported that “no seroconversions occurred among exposed partners”.26 According to one of the best known HIV/AIDS experts, Jaap Goudsmit, for heterosexual “HIV transmission” anywhere in the world, including Haiti, Africa, Thailand, “a homosexual or anal factor seems to be required”.24 In other words, at present there is ample evidence that sex plays an important role in the acquisition of a positive antibody test and AIDS and the practice of safe sex should form the basis for any effort in prevention. However, there is no proof that AIDS is a bidirectionally sexually transmitted disease. Unlike any other sexually transmitted disease, AIDS and a positive antibody test, like pregnancy, can be sexually acquired but not sexually transmitted. The difference is that while pregnancy can be acquired by a single sexual intercourse, for AIDS to appear a very high frequency of receptive anal intercourse over a long period is necessary. AIDS is more like anal 27, 28 and cervical cancer.29 The effect is not the result of the act itself but its high frequency. However, as with pregnancy, cervical and anal cancer, other factors may promote or militate against the development of AIDS and a positive antibody test.

If a hypothesis cannot account for the phenomena for which was put forward, and if its predictions are not fulfilled, then scientists have no choice but to reappraise it.

REFERENCES

1. Papadopulos-Eleopulos, E., et al. Curr. Med. Res. Opinion 15, 1s-45s (1999).
2. Gold, T. J.Sci. Exp. 3, 103-112 (1989).
3. Ioannidis, J.P. JAMA 279, 281-6 (1998).
4. Redfield, R.R. & Burke, D.S. Sci. Am. 259, 70-78 (1988).
5. Beral, V., Peterman, T.A., Berkelman, R.L. & Jaffe, H.W. Lancet 335, 123-128 (1990).
6. Shaw, M.S., Wong-Staal, F. & Gallo, R.C. in AIDS Etiology, Diagnosis, Treatment and Prevention (eds. DeVita, V.T., Hellman, S. & Rosenberg, S.A.) (J.B. Lippincott Company, Philadelphia, 1988).
7. Ludlam, C.A., et al. Lancet II, 233-236 (1985).
8. Jason, J.M., et al. JAMA 255, 212-215 (1986).
9. Montagnier, L. Ann. Int. Med. 103, 689-693 (1985).
10. Rosenberg, Y.J., Anderson, A.O. & Pabst, R. Immunol. Today 19, 10-7 (1998).
11. Hellerstein, M., et al. Nat. Med. 5, 83-89 (1999).
12. Marodon, G., Warren, D., Filomio, M.C. & Posnett, D.N. Proc. Nat. Acad. Sci. USA 96, 11958-63 (1999).
13. Katzenstein, D.A., et al. NEJM 335, 1091-8 (1996).
14. Grossman, Z., Herberman, R.B., Vatnik, N. & Intrator, N. J. Acquir. Immun. Def. Sydnr. Hum. Retrovirol. 17, 450-7 (1998).
15. Zaunders, J.J., et al. J. Inf. Dis. 180, 320-329 (1999).
16. Papadopulos-Eleopopulos, E., et al. J. Inf. Dis. 181, 1518-1519 (2000).
17. Galli, M., et al. AIDS 12, 2500-2 (1998).
18. CDC. CDC Fact sheet on HIV/AIDS Prevention January (1994).
19. Goedert, J.J., et al. Lancet 2, 711-6 (1984).
20. Stevens, C.E., et al. JAMA 255, 2167-2172 (1986).
21. Kingsley, L.A., et al. Lancet i, 345-348 (1987).
22. Palenicek, J., et al. J Acquir Immune Defic Syndr 5, 1204-11 (1992).
23. Moss, A.R., et al. Am. J. Epidemiol. 125, 1035-47 (1987).
24. Goudsmit, G. Viral Sex-The Nature of AIDS (Oxford University Press, New York, 1997).
25. Caceres, C.F. & van Griensven, G.J.P. AIDS 8, 1051-1061 (1994).
26. Padian, N.S., Shiboski, S.C., Glass, S.O. & Vittinghoff, E. Am. J. Epidemiol. 146, 350-357 (1997).
27. Daling, J.R., et al. NEJM 317, 973-7 (1987).
28. Kondlapoodi, P. JAMA 248, 2114-5 (1982).
29. Reid, B.L., French, P.W., Singer, A., Hagan, B.E. & Coppleson, M. Lancet 2, 60-2 (1978).