Abstract
The immunodeficiency virus, type 1 (HIV-1), which is the cause of the acquired immunodeficiency syndrome (AIDS), is a retrovirus of the human T-cell leukemia/lymphoma line. Well-documented quantitative and qualitative decrements in immunologic functioning occur during the course of HIV-1 spectrum disease (1,2,3). Because the HIV-1 infected person typically goes through several stages of progressive quantitative and qualitative decrements in immunologic functioning that may be associated with disease progression over many years, the disease is increasingly being viewed as a chronic disorder. Subsequent to a brief, frequently unrecognized, acute phase lasting a few weeks, the HIV-1 infected individual enters a clinically latent period characterized by low viral expression. The usual period from onset of acute infection to seropositivity (seroconversion) is 4–12 wks (4,5). After seroconversion, the clinically latent phase of seropositivity begins and may last as long as 10–15 years (6). Then, as the disease progresses, a loss in overall immunocompetence leaves the HIV-1 infected individual susceptible to opportunistic infections. These infections commonly include Pneumocystis carnii pneumonia, cryptococcal meningitis and toxoplasmosis-related phenomena, including meningoencephalitis, candidal esophagitis, and herpes simplex encephalitis.