Acquired immunodeficiency syndrome, opportunistic infections, and malignancies in male homosexuals. A hypothesis of etiologic factors in pathogenesis Academic Article Article uri icon


MeSH Major

  • DNA
  • Genome-Wide Association Study
  • Nucleic Acid Amplification Techniques
  • Premature Birth
  • Specimen Handling


  • The acquired immunodeficiency syndrome (AIDS) occurs in a subgroup of male homosexuals having sexual contact with a large number of partners. Uncommonly, AIDS has also been diagnosed in Haitians, hemophiliacs, and intravenous drug users and their infants. Manifestations include autoimmune disturbances, opportunistic infections, Kaposi's sarcoma, chronic lymphadenomegaly, non-Hodgkin's lymphoma, or squamous cell carcinoma. The hypothesis receiving most consideration is that a yet-to-be-identified virus causes AIDS. An alternative view is that repeated sexual involvement with multiple partners, in a subgroup of male homosexuals, exposes the men to the immunosuppressive impact of cytomegalovirus (CMV) and allogeneic semen. Antibody to asialo-Gm1 and other antigens on sperm react with and impair lymphoid cells. We propose a biphasic process. First, a reversible acquisition phase of impaired T-cell immunoregulation permits reactivation of Epstein-Barr virus (EBV), and autoantibodies are produced by the activated B cells. If sexual activity continues at a high level, accumulating immune defects, including destruction of thymic epithelium, lead to a second, self-sustaining phase wherein cytotoxic lymphocytes fail to eliminate herpesvirus-infected cells. Evidence is mounting that Kaposi's sarcoma is caused by CMV and that EBV is responsible for the B-cell lymphomas in these patients. Multiple factors, rather than a novel virus, probably induce AIDS in male homosexuals. If this hypothesis is correct, then rational bases for prevention and intervention can be designed.

publication date

  • January 1983



  • Academic Article


Digital Object Identifier (DOI)

  • 10.1001/jama.249.17.2370

PubMed ID

  • 6300480

Additional Document Info

start page

  • 2370

end page

  • 4


  • 249


  • 17