Infectious AIDS – Stretching the Germ Theory Beyond Its Limits

Abstract

The hypothesis that human immunodeficiency virus (HIV) causes AIDS was advanced in 1984, based only on circumstantial evidence. To this date, the primary evidence are correlations between the presence of antibody against HIV and AIDS. But these correlations are biased by proponents of the HIV hypothesis in favour of HIV. They ignore HIV-free AIDS and they base correlations on selected studies because there are no national HIV-AIDS statistics. The HIV-AIDS hypothesis has made the following predictions: (I) AIDS would ‘explode’ from the original risk groups into the general population via sexual transmission of HIV (2) Health care workers would contract AIDS from their patients, scientists from propagating HIV, and prostitutes from their clients. (3) The 150 chimpanzees that have been experimentally inoculated with HIV, and the 15,000 American hemophiliacs who have been iatrogenically inoculated before 1984, would develop AIDS. (4) Antiviral immunity and vaccines would protect against AIDS. (5) HIV would cause AIDS by killing T-cells. (6) AIDS would occur only in people infected by HIV. But none of these predictions proved to be correct. Recent studies show that HIV is a passenger virus instead of the cause of AIDS: (1) AIDS occurs at unpredictable intervals after infection; (2) HIV may be active, passive, or totally absent from otherwise identical AIDS cases. Indeed, AIDS does not meet one of the classical criteriy of infectious disease: (1) Equal distribution between the sexes; (2) disease following infection within days or weeks, the time microbes take to become either immunogenic or pathogenic or both; (3) the presence of a common active microbe. Therefore it is proposed that American and European AIDS is caused by the long-term consumption of recreational drugs and the anti-HIV drug AZT This hypothesis is testable and provides a rational basis for AIDS control.

Foreign-protein-mediated immunodeficiency in hemophiliacs with and without HIV

“…All of the above associations between HIV and AIDS support the hypothesis that HIV is a passenger virus, instead of the cause of AIDS (Duesberg, 1994). A passenger virus differs from one that causes a disease in three criteria:…”

“…Instead, most T-cells are lost when the virus is least active or latent in hemophiliacs (Phillips et al, 1994a) and other risk grous (Duesberg, 1992a;1993aPiatak et aL, 1993;Sheppard, Ascher & Krowka, 1993), namely after it is neutralized by antiviral immunity (a positive H!V-antibody test). Indeed, there are healthy, HIV-antibody positive persons in which 33 to 43 times more cells are infected by latent HIV than in AIDS patients (Simmonds et al, 1990;Bagasra et al, 1992;Duesberg, 1994). Even Gallo, who claims credit for the HIV-AIDS hypothesis (Gallo et al, 1984), has recently acknowledge: 'I think that if HIV is not being expressed and not reforming virus and replicating, the virus is a dud, and won't be causing the disease.., nobody is saying that indirect control of the virus is not important...' (Jones, 1994).…”

“…In the case of AIDS, over 4621 HIVfree AIDS cases have been clinically diagnosed (Duesberg, 1993b; see also Section 4.6). Therefore, HIV meets each of the classical criteria of a passenger virus --exactly (Duesberg, 1994).…”

“…Moreover, since HIV is not active in most AIDS patients, and often more active in healthy carriers than in AIDS patients (Duesberg, 1993a(Duesberg, , 1994Piatak et al, 1993), and since AIDS patients with and without HIV are clinically identical (Duesberg, 1993b), HIV is in fact only a harmless passenger virus. It is harmless, because it does not contribute secondary diseases to AIDS pathogenicity, as for example pneumocystis pneumonia, candida or herpes virus do.…”

“…These microbes each cause typical AIDS-defining opportunistic infections. But HIV does not appreciably affect the pathogenicity of AIDS as HIV-free and HIVpositive AIDS cases are clinically indistinguishable (Duesberg, 1993b(Duesberg, , 1994. Likewise, there is no clinical distinction between AIDS cases in which HIV is active and those in which it is totally latent and restricted to very few cells (Duesberg, 1993a;Piatak et al, 1993).…”