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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Badley, A. D. Articles by Lynch, D. H. Search for Related Content PubMed PubMed Citation Articles by Badley, A. D. Articles by Lynch, D. H. Related Collections Immunobiology Apoptosis Review Articles Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 November 2000, Vol. 96, No. 9, pp. 2951-2964 REVIEW ARTICLE Mechanisms of HIV-associated lymphocyte apoptosis Andrew D. Badley, André A. Pilon, Alan Landay, and David H. Lynch From the Ottawa Hospital Research Institute and the Division of Infectious Diseases, Ottawa Hospital, Ottawa, Ontario, Canada; Department of Immunology/Microbiology, Rush Medical College, Chicago, IL; and Immunex Corporation, Seattle, WA. Infection with the human immunodeficiency virus (HIV) is associated with a progressive decrease in CD4 T-cell number and a consequent impairment in host immune defenses. Analysis of T cells from patients infected with HIV, or of T cells infected in vitro with HIV, demonstrates a significant fraction of both infected and uninfected cells dying by apoptosis. The many mechanisms that contribute to HIV-associated lymphocyte apoptosis include chronic immunologic activation; gp120/160 ligation of the CD4 receptor; enhanced production of cytotoxic ligands or viral proteins by monocytes, macrophages, B cells, and CD8 T cells from HIV-infected patients that kill uninfected CD4 T cells; and direct infection of target cells by HIV, resulting in apoptosis. Although HIV infection results in T-cell apoptosis, under some circumstances HIV infection of resting T cells or macrophages does not result in apoptosis; this may be a critical step in the development of viral reservoirs. Recent therapies for HIV effectively reduce lymphoid and peripheral T-cell apoptosis, reduce viral replication, and enhance cellular immune competence; however, they do not alter viral reservoirs. Further understanding the regulation of apoptosis in HIV disease is required to develop novel immune-based therapies aimed at modifying HIV-induced apoptosis to the benefit of patients infected with HIV. © 2000 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: N. Gasper-Smith, D. M. Crossman, J. F. Whitesides, N. Mensali, J. S. Ottinger, S. G. Plonk, M. A. Moody, G. Ferrari, K. J. Weinhold, S. E. Miller, et al. 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