chapter  17
12 Pages

HIV-Associated Dementia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Human Immunodeficiency Virus (HIV)/Acquired

ByDavid B. Clifford, Mary Gould

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).