Factor VIII, HIV and AIDS in haemophiliacs: An analysis of their relationship

Papadopulos-Eleopulos, Eleni; Turner, Valendar F.; Papadimitriou, John; Causer, David

doi:10.1007/bf01435000

Genetica

1995

DOI: 10.1007/bf01435000

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Factor VIII, HIV and AIDS in haemophiliacs: An analysis of their relationship

Eleni Papadopulos-Eleopulos

Valendar F. Turner

John Papadimitriou

et al.

Abstract: In this review, the association between the Acquired Immune Deficiency Syndrome (AIDS) and haemophilia has been carefully examined, especially the data that have been interpreted as indicating transmission of the human immunodeficiency virus (HIV) to the recipients of purportedly contaminated factor VIII preparations. In our view, the published data do not prove the hypothesis that such transmission occurs, and therefore HIV cannot account for AIDS in haemophiliacs.

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Cited by 3 publications

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

Duesberg

1995

Genetica

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Hemophilia-AIDS has been interpreted in terms of two hypotheses: the foreign-protein-AIDS hypothesis and the Human Immunodeficiency Virus (HIV)-AIDS hypothesis. The foreign-protein-AIDS hypothesis holds that proteins contaminating commercial clotting factor VIII cause immunosuppression. The foreign-protein hypothesis, but not the HIV hypothesis, correctly predicts seven characteristics of hemophilia-AIDS: 1) The increased life span of American hemophiliacs in the two decades before 1987, although 75% became infected by HIV--because factor VIII treatment, begun in the 1960s, extended their lives and simultaneously disseminated harmless HIV. After 1987 the life span of hemophiliacs appears to have decreased again, probably because of widespread treatment with the cytotoxic anti-HIV drug AZT. 2) The distinctly low, 1.3-2%, annual AIDS risk of hemophiliacs, compared to the higher 5-6% annual risk of intravenous drug users and male homosexual aphrodisiac drug users--because transfusion of foreign proteins is less immunosuppressive than recreational drug use. 3) The age bias of hemophilia-AIDS, i.e. that the annual AIDS risk increased 2-fold for each 10-year increase in age--because immunosuppression is a function of the lifetime dose of foreign proteins received from transfusions. 4) The restriction of hemophilia-AIDS to immunodeficiency diseases--because foreign proteins cannot cause non-immunodeficiency AIDS diseases, like Kaposi's sarcoma. 5) The absence of AIDS diseases above their normal background in sexual partners of hemophiliacs--because transfusion-mediated immunotoxicity is not contagious. 6) The occurrence of immunodeficiency in HIV-free hemophiliacs--because foreign proteins, not HIV, suppress their immune system. 7) Stabilization, even regeneration, of immunity of HIV-positive hemophiliacs by long-term treatment with pure factor VIII. This shows that neither HIV nor factor VIII plus HIV are immunosuppressive by themselves. Therefore, AIDS cannot be prevented by elimination of HIV from the blood supply and cannot be rationally treated with genotoxic antiviral drugs, like AZT. Instead, hemophilia-AIDS can be prevented and has even been reverted by treatment with pure factor VIII.

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

Duesberg

1995

Genetica

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A Critical Analysis of the Pharmacology of AZT and its Use in AIDS

Papadopulos-Eleopulos¹,

Turner

Papadimitriou

et al. 1999

Current Medical Research and Opinion

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The triphosphorylated form of the nucleoside analogue 3'-azido-3'-deoxythymidine (Zidovudine, AZT) is claimed to interrupt the HIV replication cycle by a selective inhibition of viral reverse transcriptase, thereby preventing the formation of new proviral DNA in permissive, uninfected cells. Given that initial HIV infection of an individual instigates abundant HIV replication from inception until death, and that the life of infected T-cells is only several days, the administration of AZT should lead both in vitro and in vivo (i) to decreased formation of proviral DNA; and thus (ii) to decreased frequencies of 'HIV isolation' (detection of p24 or reverse transcription or both) in stimulated cultures/cocultures of T-cells from seropositive individuals; (iii) to decreased synthesis of HIV p24 and RNA ('antigenaemia', 'plasma viraemia', 'viral load') ultimately resulting in low or absent levels of all three parameters; and (iv) to a perfect and direct correlation between all these parameters. A critical analysis of the presently available data shows that no such evidence exists, an outcome not unexpected given the pharmacological data on AZT. HIV experts all agree that only the triphosphorylated form of AZT (AZTTP) and not the unphosphorylated form administered to patients, nor its mono- or diphosphate, is the active agent. Furthermore, the mechanism of action is the ability of AZTTP to halt the formation of HIV-DNA (chain termination). However, although this claim was posited from the outset, AZT underwent clinical trials and was introduced as a specific anti-HIV drug many years before there were any data proving that the cells of patients are able to triphosphorylate the parent compound to a level considered sufficient for its putative pharmacological action. Notwithstanding, from the evidence published since 1991 it has become apparent that no such phosphorylation takes place and thus AZT cannot possess an anti-HIV effect. However, the scientific literature does elucidate: (i) a number of biochemical mechanisms which predicate the likelihood of widespread, serious toxicity from use of this drug; (ii) in vitro data proving that AZT has significant antibacterial and antiviral properties which confound interpretation of its effects when administered to patients. Based on all these data it is difficult if not impossible to explain why AZT was introduced and still remains the most widely recommended and used anti-HIV drug.

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The Viral Model for AIDS: Paradigmatic Dominance, Politics, or Best Approximation of Reality?

Pezza

1995

Int Q Community Health Educ

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In 1981, a non-infectious disease hypothesis was offered by the Centers for Disease Control to explain the cluster of atypical pneumonias which had appeared among gay men in the United States. Although quickly supplanted by the now widely held viral hypothesis and largely ignored by professional and media sources, that view has persisted. This article raises the question of why one explanation for the epidemic of immune system suppression has dominated the discourse on AIDS, despite the anomalies attributed to it by the proponents of other viewpoints. Alternative responses to the question are set forth drawing upon literatures in the philosophy of science and public policy formulation. Some discussion is provided of what the consequences may be if one of the contrarian hypotheses proves to be the closer approximation to the truth about AIDS etiology.

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Factor VIII, HIV and AIDS in haemophiliacs: An analysis of their relationship

Cited by 3 publications

References 143 publications

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

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

A Critical Analysis of the Pharmacology of AZT and its Use in AIDS

The Viral Model for AIDS: Paradigmatic Dominance, Politics, or Best Approximation of Reality?

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