Advertisement
Research Article Free access | 10.1172/JCI115188
Department of Medicine, University of California at San Diego, La Jolla 92093.
Find articles by Terai, C. in: JCI | PubMed | Google Scholar
Department of Medicine, University of California at San Diego, La Jolla 92093.
Find articles by Kornbluth, R. in: JCI | PubMed | Google Scholar
Department of Medicine, University of California at San Diego, La Jolla 92093.
Find articles by Pauza, C. in: JCI | PubMed | Google Scholar
Department of Medicine, University of California at San Diego, La Jolla 92093.
Find articles by Richman, D. in: JCI | PubMed | Google Scholar
Department of Medicine, University of California at San Diego, La Jolla 92093.
Find articles by Carson, D. in: JCI | PubMed | Google Scholar
Published May 1, 1991 - More info
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.
Images.