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Research Article Free access | 10.1172/JCI115188

Apoptosis as a mechanism of cell death in cultured T lymphoblasts acutely infected with HIV-1.

C Terai, R S Kornbluth, C D Pauza, D D Richman, and D A Carson

Department of Medicine, University of California at San Diego, La Jolla 92093.

Find articles by Terai, C. in: PubMed | Google Scholar

Department of Medicine, University of California at San Diego, La Jolla 92093.

Find articles by Kornbluth, R. in: PubMed | Google Scholar

Department of Medicine, University of California at San Diego, La Jolla 92093.

Find articles by Pauza, C. in: PubMed | Google Scholar

Department of Medicine, University of California at San Diego, La Jolla 92093.

Find articles by Richman, D. in: PubMed | Google Scholar

Department of Medicine, University of California at San Diego, La Jolla 92093.

Find articles by Carson, D. in: PubMed | Google Scholar

Published May 1, 1991 - More info

Published in Volume 87, Issue 5 on May 1, 1991
J Clin Invest. 1991;87(5):1710–1715. https://doi.org/10.1172/JCI115188.
© 1991 The American Society for Clinical Investigation
Published May 1, 1991 - Version history
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Abstract

The mechanisms by which HIV-1 infection kills T lymphocytes are not clearly established. Apoptosis is an internally programmed cell death pathway that may regulate both T cell development and senescence, and that is characterized by cleavage of DNA at internucleosomal regions. The present experiments show that acute HIV-1 infection of MT2 lymphoblasts and activated normal peripheral blood mononuclear cells induces apoptosis. The addition of anti-gp120 neutralizing antibody, after HIV-1 infection of MT2 cells, permitted sustained high levels of viral replication, but blocked apoptosis and cell death. Apoptosis may account for the direct cytopathologic effects of HIV-1 in T cells.

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