PubMed:9334723 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PubMed/sourceid/9334723","sourcedb":"PubMed","sourceid":"9334723","source_url":"http://www.ncbi.nlm.nih.gov/pubmed/9334723","text":"HIV-1 Vpr suppresses immune activation and apoptosis through regulation of nuclear factor kappa B.\nThe HIV-1 accessory gene product Vpr can influence viral pathogenesis by affecting viral replication as well as host cell transcription and proliferation. We have investigated the effects of Vpr on host cell activation and confirm that it influences cellular proliferation. However, we have also found that Vpr modulates T-cell receptor (TCR)-triggered apoptosis in a manner similar to that of glucocorticoids. In the absence of TCR-mediated activation, Vpr induces apoptosis whereas in its presence, Vpr interrupts the expected induction of apoptosis. This regulation of apoptosis is linked to Vpr suppression of NF-kappa B activity via the induction of I kappa B, an inhibitor of NF-kappa B. 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Our finding that Vpr can regulate NF-kappa B supports the hypothesis that some aspects of viral pathogenesis are the consequence of cell dysregulation by 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