AIDS: AN EXPLANATION FOR ITS OCCURRENCE AMONG HOMOSEXUAL MEN NLM AIDSLINE Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.

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AIDS: AN EXPLANATION FOR ITS OCCURRENCE AMONG HOMOSEXUAL MEN

Aids and Infections of Homosexual Men. Second Edition. Ma P and Armstrong D, eds. Boston, Butterworths, p. 449-70 1989.. Unique Identifier : AIDSLINE ICDB/90659654
Sonnabend JA; Dept. of Pediatrics, St. Luke's-Roosevelt Medical Center, New; York, NY


Abstract: A model is presented to explain the pathogenesis of AIDS in homosexual men; it does not require the participation of HIV or any other novel agent. The essential element of the model is that AIDS pathogenesis is an interactive, multifactorial process resulting from repeated exposures, particularly rectally, to large inocula of cytomegalovirus (CMV), together with repeated exposures to multiple alloantigens contained in semen, and repeated exposures to other sexually transmitted pathogens, including Treponema pallidum. These exposures result in a cumulative impairment of cytotoxic responses against intracellular parasites, including CMV and other herpesviruses. Reactivation of Epstein-Barr virus (EBV) is an important part of the model, and a two-stage process for the development of AIDS is involved: an initial stage of disease acquisition associated with repeated exposures to environmental factors, followed by a self-perpetuating stage that no longer requires these exposures and has features of a positive feedback system. There is also a role for interferon (IFN) and possibly for tumor necrosis factor in the pathogenesis. Factors of probable etiologic importance include CMV and immunoregulatory defects, reactivation of EBV, polyclonal activation of B cells and autoimmunity, sustained high levels of IFN, immune responses to semen, and circulating immune complexes. Therapeutic interventions suggested by this model include removal of humoral factors such as IFN (eg, by plasmapheresis), administration of cyclophosphamide to control increased Ig production and possibly to inhibit T8 suppressor cells, and use of monoclonal antibodies to selectively remove T8 suppressor cells. (106 Refs)
Keywords: Acquired Immunodeficiency Syndrome/IMMUNOLOGY/*TRANSMISSION Antigen-Antibody Complex/ANALYSIS Autoantibodies/ANALYSIS B-Lymphocytes/IMMUNOLOGY Cytomegalovirus/PATHOGENICITY Cytomegalovirus Infections/IMMUNOLOGY CD4-Positive T-Lymphocytes/MICROBIOLOGY Herpesvirus 4, Human/PATHOGENICITY *Homosexuality Human HIV-1/*PATHOGENICITY HIV-2/*PATHOGENICITY Male Opportunistic Infections/IMMUNOLOGY Semen/IMMUNOLOGY Virus Activation MONOGRAPH REVIEWKWDacquiredimmunodeficiencysyndrome/immunology/KWDtransmissionantigen-antibodycomplex/analysisautoantibodies/analysisb-lymphocytes/immunologycytomegalovirus/pathogenicitycytomegalovirusinfections/immunologycd4-positivet-lymphocytes/microbiologyherpesvirus4,human/pathogenicityKWDhomosexualityhumanhiv-1/KWDpathogenicityhiv-2/KWDpathogenicitymaleopportunisticinfections/immunologysemen/immunologyvirusactivationmonographreview
912130
M91C4113

Copyright © 1991 - National Library of Medicine. Reproduced under license with the National Library of Medicine, Bethesda, MD.

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