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A MULTIFACTORIAL MODEL FOR THE DEVELOPMENT OF AIDS IN HOMOSEXUAL MEN a
Author(s) -
Sonnabend Joseph A.,
Witkin Steven S.,
Purtilo David T.
Publication year - 1984
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1984.tb37134.x
Subject(s) - obstetrics and gynaecology , medicine , medical laboratory , gerontology , citation , annals , family medicine , library science , classics , history , pathology , genetics , biology , pregnancy , computer science
The authors present a multifactorial model for the development of acquired immunodeficiency syndrome (AIDS) in homosexual men. It is posited that there is no specific AIDS agent; rather, AIDS is conceptualized as the result of an interaction of the known or likely effects of repeated exposures to specific environmental factors. It is suggested that different pathways may lead to similar disorders of immune regulation in other groups affected by AIDS. The salient environmental factors include: repeated exposures to multiple allogenic semen, repeated infection with cytomegalovirus, and infection with other sexually transmitted pathogens. It is proposed that AIDS develops in 2 stages: a reversible stage of disease acquisition followed by a self-sustaining stage of disease progression. Promiscuity is critical to the 1st stage, since it is associated with an accumulation of effects that eventually lead to the 2nd stage. The frequency with which an individual is reexposed to cytomegalovirus is a function of the number of different sexual partners, the prevalence of cytomegalovirus carriage in the population with whose members the person interacts, and the specific nature of sexual practice (e.g., passive anal intercourse). Epstein-Barr virus plays an important role in contributing to disordered immune regulation. The central defect in the self-sustaining stage of AIDS development is an inability of cytotoxic lymphocytes to clear cells infected by cytomegalovirus as a result of both humoral factors and cellular factors. If cytotoxic function becomes further inhibited, expansion of the total cytomegalovirus antigenic load will result in further immunosuppression. Such a multifactorial model is believed to facilitate epidemiologic analysis.