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• W6771640 abstract "Human immunodeficiency virus (HIV) infection results in the progressive destruction of CD4 T lymphocytes, generally associated with disease progression. Despite years of investigation, the mechanisms responsible for the deletion of this lymphocyte subset are still not elucidated (Levy 1993; Weiss 1993; Gougeon 1995). CD4 cell destruction can be mediated directly by virus replication as a consequence of viral gene expression or indirectly by priming of uninfected cells to apoptosis when triggered by different agents. For example, Tat, a viral transcription factor, was shown to affect transciption of genes involved in cell survival. Tat was found to upregulate Bcl-2 expression, protecting cells from apoptosis (Zauli et al. 1995). In contrast, establishment of stable Tat-expressing cell lines or addition of exogenous Tat have been reported to sensitize cells to CD95-, anti-T-cell receptor (TCR)- and anti-CD4-induced apoptosis (Li et al. 1995; Westendorp et al. 1995). Vpr gene, required for productive infection of non-dividing cells (Hattori et al. 1990), was also recently found to induce apoptosis by blocking the cell cycle in the G2 phase (Bartz et al. 1996; Steward et al. 1997). The cytopathic effect of HIV in CD4 T cell cultures, manifested by ballooning of cells and formation of syncytia, was shown to be associated with apoptosis (Laurent-Crawford et al. 1991; Terai et al. 1991)." @default.
• W6771640 created "2016-06-24" @default.
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• W6771640 date "1998-01-01" @default.
• W6771640 modified "2023-10-14" @default.
• W6771640 title "T Cell Apoptosis in HIV Infection: Mechanisms and Relevance for AIDS Pathogenesis" @default.
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• W6771640 doi "https://doi.org/10.1007/978-3-540-69185-3_11" @default.
• W6771640 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9949839" @default.
• W6771640 hasPublicationYear "1998" @default.
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