On the Structure of the Epidemic Spread of AIDS: The Influence of an Infectious Coagent

Weyer, Jürgen; Eggers, Hans J.

doi:10.1016/s0934-8840(11)80239-2

Cited by 12 publications

(14 citation statements)

References 9 publications

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“…as well. The implications of multipathogen complexes involving complementary antigens on the pathogenesis and spread of AIDS may require significant rethinking since paired infections behave epidemiologically and immunologically differently than single infections (RootBernstein and Merrill, 1997;Weyer and Eggers, 1990).…”

Section: Discussionmentioning

confidence: 99%

Antigenic complementarity among AIDS-associated infectious agents and molecular mimicry of lymphocyte proteins as inducers of lymphocytotoxic antibodies and circulating immune complexes

Root‐Bernstein

2004

Journal of Clinical Virology

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Section: Discussionmentioning

confidence: 99%

Antigenic complementarity among AIDS-associated infectious agents and molecular mimicry of lymphocyte proteins as inducers of lymphocytotoxic antibodies and circulating immune complexes

Root‐Bernstein

2004

Journal of Clinical Virology

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“…This view is incontrovertible" (Goudsmit, 1992). Likewise, the epidemiologists Eggers and Weyer conclude that "the spread of AIDS does not behave like the spread of a disease that is caused by a single sexually transmitted agent" (Eggers and Weyer, 1991) and hence have "simulated a cofactor [that] cannot be identified with any known infectious agent" (Weyer and Eggers, 1990). Anderson and May (1992) had to invent "assortative scenarios" for different AIDS risk groups to reconcile AIDS with infectious disease.…”

Section: Aids Not Compatible With Infectious Diseasementioning

confidence: 99%

“…These findings argue against a sexually transmitted cause, because sexual transmission predicts a much higher AIDS risk for homosexuals with hundreds of sexual partners than for intravenous drug users (Section 4) (Weyer and Eggers, 1990;Eggers and Weyer, 1991). Indeed, numerous controlled studies have indicated that the morbidity and mor-tality of intravenous drug users is independent of HIV (Sections 4.4, 4.5 and 4.7).…”

Section: Annual Aids Risks Of Different Hiv-infected Risk Groups Incmentioning

confidence: 99%

Aids acquired by drug consumption and other noncontagious risk factors

Duesberg

1992

Pharmacology & Therapeutics

125

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The hypothesis that human immunodeficiency virus (HIV) is a new, sexually transmitted virus that causes AIDS has been entirely unproductive in terms of public health benefits. Moreover, it fails to predict the epidemiology of AIDS, the annual AIDS risk and the very heterogeneous AIDS diseases of infected persons. The correct hypothesis must explain why: (1) AIDS includes 25 previously known diseases and two clinically and epidemiologically very different epidemics, one in America and Europe, the other in Africa; (2) almost all American (90%) and European (86%) AIDS patients are males over the age of 20, while African AIDS affects both sexes equally; (3) the annual AIDS risks of infected babies, intravenous drug users, homosexuals who use aphrodisiacs, hemophiliacs and Africans vary over 100-fold; (4) many AIDS patients have diseases that do not depend on immunodeficiency, such as Kaposi's sarcoma, lymphoma, dementia and wasting; (5) the AIDS diseases of Americans (97%) and Europeans (87%) are predetermined by prior health risks, including long-term consumption of illicit recreational drugs, the antiviral drug AZT and congenital deficiencies like hemophilia, and those of Africans are Africa-specific. Both negative and positive evidence shows that AIDS is not infectious: (1) the virus hypothesis fails all conventional criteria of causation; (2) over 100-fold different AIDS risks in different risk groups show that HIV is not sufficient for AIDS; (3) AIDS is only 'acquired,' if at all, years after HIV is neutralized by antibodies; (4) AIDS is new but HIV is a long-established, perinatally transmitted retrovirus; (5) alternative explanations disprove all assumptions and anecdotal cases cited in support of the virus hypothesis; (6) all AIDS-defining diseases occur in matched risk groups, at the same rate, in the absence of HIV; (7) there is no common, active microbe in all AIDS patients; (8) AIDS manifests in unpredictable and unrelated diseases; and (9) it does not spread randomly between the sexes in America and Europe. Based on numerous data documenting that drugs are necessary for HIV-positives and sufficient for HIV-negatives to develop AIDS diseases, it is proposed that all American/European AIDS diseases, that exceed their normal background, result from recreational and anti-HIV drugs. African AIDS is proposed to result from protein malnutrition, poor sanitation and subsequent parasitic infections. This hypothesis resolves all paradoxes of the virus-AIDS hypothesis. It is epidemiologically and experimentally testable and provides a rational basis for AIDS control.

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“…Weyer and Eggers (1990), for example, show that even if one assumes the rates of AIDS onset to be the same for each risk group, the 'drastic overrepresentation of the sexually highly active groups and drug abusers in the number of AIDS cases obviously requires that the transmission of AIDS unequivocally depends on the sexual and drug risk ... In fact, several mathematical models of AIDS epidemiology demonstrate that the observed rates of development in each risk group can be explained only by models involving two or more synergistic agents.…”

Section: Myth 1: Hiv Progresses To Aids At the Same Rate In All Risk mentioning

confidence: 99%

Five myths about AIDS that have misdirected research and treatment

Root‐Bernstein

1995

Genetica

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A number of widely repeated and factually incorrect myths have pervaded the AIDS research literature, misdirecting research and treatment. Five of the most outstanding are: 1) that all risk groups develop AIDS at the same rate following HIV infection; 2) that there are no true seroreversions following HIV infection; 3) that antibody is protective against HIV infection; 4) that the only way to treat AIDS effectively is through retroviral therapies; and 5) that since HIV is so highly correlated with AIDS incidence, it must be the sole necessary and sufficient cause of AIDS. A huge body of research, reviewed in this paper, demonstrates the falsity of these myths. 1) The average number of years between HIV infection and AIDS is greater than 20 years for mild hemophiliacs, 14 years for young severe hemophiliacs, 10 years for old severe hemophiliacs, 10 years for homosexual men, 6 years for transfusion patients of all ages, 2 years for transplant patients, and 6 months for perinatally infected infants. These differences can only be explained in terms of risk-group associated cofactors. 2) Seroreversions are common. Between 10 and 20 percent of HIV-seronegative people in high risk groups have T-cell immunity to HIV, and may have had one or more verified positive HIV antibody tests in the past. 3) Antibody, far from being protective against HIV, appears to be highly diagnostic of loss of immune regulation of HIV, and some evidence of antibody-enhancement of infection exists. 4) Non-retroviral treatments of HIV infection, including safer sex practices, elimination of drug use, high nutrient diets, and limited reexposure to HIV and its cofactors have proven to be effective means of preventing or delaying onset of AIDS. 5) Many immunosuppressive factors, including drug use, multiple concurrent infections, and exposure to alloantigens, are as highly correlated with AIDS risk groups as HIV. These data are more consistent with AIDS being a multifactorial or synergistic disease than a monofactorial one.

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On the Structure of the Epidemic Spread of AIDS: The Influence of an Infectious Coagent

Cited by 12 publications

References 9 publications

Antigenic complementarity among AIDS-associated infectious agents and molecular mimicry of lymphocyte proteins as inducers of lymphocytotoxic antibodies and circulating immune complexes

Antigenic complementarity among AIDS-associated infectious agents and molecular mimicry of lymphocyte proteins as inducers of lymphocytotoxic antibodies and circulating immune complexes

Aids acquired by drug consumption and other noncontagious risk factors

Five myths about AIDS that have misdirected research and treatment

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