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Regulation of HIV-1 Gene Expression

Regulation of HIV-1 Gene Expression 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 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annual Review of Immunology Annual Reviews

Regulation of HIV-1 Gene Expression

Annual Review of Immunology , Volume 8 (1) – Apr 1, 1990

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Publisher
Annual Reviews
Copyright
Copyright 1990 Annual Reviews. All rights reserved
Subject
Review Articles
ISSN
0732-0582
eISSN
1545-3278
DOI
10.1146/annurev.iy.08.040190.002321
pmid
2188670
Publisher site
See Article on Publisher Site

Abstract

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

Journal

Annual Review of ImmunologyAnnual Reviews

Published: Apr 1, 1990

Keywords: AIDS; Tat; Rev; Nef; transcription; viral latency

There are no references for this article.