Recognition of the global epidemic now known as HIV/AIDS began in 1981 with the report of five cases of Pneumocystis carinii pneumonia (PCP) in young, previously healthy men living in California (1). At that time a rare infection, PCP occurred only in the setting of underlying immune deficiency. This event, and subsequent reports of sudden increases in the incidence of other opportunistic conditions, such as Kaposi’s sarcoma, fungal infections, and mycobacterial infections, touched off a scientific inquiry that led to the identification in 1983 of the HIV-1 virus. The virus was found to be a retrovirus, characterized by transcription of the RNA genome into DNA in host cells. It is a member of the subgroup of lentiviruses, so named because of their generally indolent course of infection (2). Pathogenic features of lentiviruses include specificity for cells of the immune system (for HIV, CD4 lymphocytes and monocytes), a prolonged asymptomatic period, and neurological damage. In these respects, HIV-1 bears similarities to other lentiviruses, including visna (which causes a demyelinating encephalomyelitis in sheep), simian immunodeficiency virus (which causes a condition similar to AIDS in monkeys), caprine arthritis encephalitis virus, and feline immunodeficiency virus (3).