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The type-I human immunodeficiency virus (HIV-I) has been clearly impli cated as the primary cause of the acquired immune deficiency syndrome (AIDS) (1, 2). The cytopathic effects of HIV -I within CD4-expressing T cells in vivo lead to the progressive depletion of this essential lymphocyte subset (1-4). In addition to this lethal immunodeficiency, HIV-l has also been linked clinically with an even broader array of pathological processes including Kaposi's sarcoma, progressive central nervous system degener ation, and aggressive non-Hodgkin's B-cell lymphomas (3, 4). Major recog nized risk factors for HIV-l infection in the United States include male homosexuality, intravenous drug abuse, and transfusion exposure to con taminated blood or blood products (5). Recent studies suggest that over one million individuals have been infected with HIV-I in the United States, while at least fifty thousand patients have developed AIDS (5). In sharp contrast to the high risk groups identified within the United States and Europe, however, HIV-I infection in equatorial Africa has spread widely within the heterosexual population (6). AIDS and the related HIV-l syn dromes clearly represent a major international health crisis given the epidemic nature of its spread. The successful design of effective therapies to prevent or
Annual Review of Immunology – Annual Reviews
Published: Apr 1, 1990
Keywords: AIDS; Tat; Rev; Nef; transcription; viral latency
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