ABSTRACT
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).
