Infection with human immunodeficiency virus (HIV) causes an extensive array of immunologic abnormalities which ultimately lead to severe immunosuppression, opportunistic disease, and death. Many of the immunologic defects can be attributable to the quantitative and qualitative deficiencies of T4 lymphocytes caused by HIV. Other abnormalities may reflect chronic HIV exposure to or infection of other immunologic cells including B cells and monocyte/macrophages. A summary of the potential mechanisms of pathogenesis of HIV infection is shown in fig. 2. One of the most puzzling aspects of infection with HIV is the length and variability of time between initial infection and disease. It appears that activation of latent or chronic, smoldering infection into active disease may be the result of a variety of factors, including heterologous viruses and cytokines, whose common denominator is the ability to induce the production of DNA-binding proteins that interact with the HIV-LTR and induce transcription of virus.