Abstract
Normal immature thymocytes respond to activation by undergoing programmed cell death (apoptosis), a physiological deletion mechanism involved in the selection of the T-cell repertoire. In this article, Jean Claude Ameisen and André Capron suggest that inappropriate induction of a form of programmed T-cell death could account for both qualitative and quantitative helper T-cell defects of HIV-infected patients. A model of AIDS pathogenesis is presented that may explain several features of HIV infection, including evolution of the disease and the development of defects in nonimmunological organs.
MeSH terms
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AIDS Dementia Complex / pathology
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Acquired Immunodeficiency Syndrome / pathology*
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CD4-Positive T-Lymphocytes / drug effects
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CD4-Positive T-Lymphocytes / immunology
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CD4-Positive T-Lymphocytes / pathology*
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Cell Survival* / drug effects
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Endodeoxyribonucleases / biosynthesis
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Endodeoxyribonucleases / physiology
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Gene Expression Regulation
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HIV / physiology
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HIV Envelope Protein gp120 / physiology
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Hematopoietic Stem Cells / pathology
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Lymphocyte Activation / drug effects
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Mitogens / pharmacology
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Models, Biological
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Signal Transduction
Substances
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HIV Envelope Protein gp120
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Mitogens
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Endodeoxyribonucleases