The clinical manifestations of chronic infection with the Human Immunodeficiency Virus (HIV) fall into two broad categories: opportunistic infections and opportunistic malignancies. The initial observation of both occurring in outbreak fashion among young homosexual men led to the early identification of the present pandemic. Conversely, the identification of additional malignancies which occur in excess frequency in the presence of the immunodeficiency of HIV infection can provide insight into the role of viruses in human malignancy. The first report related to the acquired immunodeficiency syndrome (AIDS) epidemic was of a series of 5 cases of Pneumocystic carinii in young homosexual men in Los Angeles and was published in June 1981. This was shortly followed by the report of additional cases of P. carinii as well as Kaposi's sarcoma (KS) occurring among young homosexual men in California and New York City. The increased risk of KS among people with HIV infection has been confirmed since these initial reports, with 1 in 5 AIDS patients in the United States developing KS sometime in their course of disease. However, the proportion of AIDS patients with KS has decreased from 35% before 1983 to 15% in the first half of 1987. Among the recognized risk groups of AIDS patients, the proportion with KS is highest among homosexual men and female intravenous drug abusers, and lowest among children and hemophiliacs. This variation suggests that risk of KS in AIDS parallels that of sexually-transmitted infections. A second family of opportunistic malignancy in AIDS is comprised of the non-Hodgkin's disease lymphomas (NHL). These lymphomas are typically of B-cell origin, immunoblastic or Burkitt's-like in character, and frequently present with extra-nodal involvement such as the central nervous system. These were first recognized somewhat later than KS as being associated with AIDS; together, KS and NHL account for about 95% of all neoplasms seen in AIDS patients. Additional malignancies are currently suspected to occur excessively with HIV infection. These include Hodgkin's disease, anorectal carcinoma, and testicular cancer. Validation of these associations will require extensive epidemiologic surveillance. Since HIV infection leads to progressive loss of cellular immunity, it is probable that these malignancies result from the progressive reactivation or loss of immunologic control of latent oncogenic viruses. The cytomegalovirus has been implicated in the pathogenesis of KS, perhaps with reinfection, and the Epstein-Barr virus in the NHL. The role of papilloma viruses in anorectal carcinoma has also been proposed.(ABSTRACT TRUNCATED AT 400 WORDS)