Cell cycle arrest by Vpr in HIV-1 virions and insensitivity to antiretroviral agents
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作者:
Poon, B
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机构:Univ Calif Los Angeles, Sch Med, Dept Microbiol & Immunol & Med, AIDS Inst, Los Angeles, CA 90095 USA
Poon, B
Grovit-Ferbas, K
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机构:Univ Calif Los Angeles, Sch Med, Dept Microbiol & Immunol & Med, AIDS Inst, Los Angeles, CA 90095 USA
Grovit-Ferbas, K
Stewart, SA
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机构:Univ Calif Los Angeles, Sch Med, Dept Microbiol & Immunol & Med, AIDS Inst, Los Angeles, CA 90095 USA
Stewart, SA
Chen, ISY
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机构:
Univ Calif Los Angeles, Sch Med, Dept Microbiol & Immunol & Med, AIDS Inst, Los Angeles, CA 90095 USAUniv Calif Los Angeles, Sch Med, Dept Microbiol & Immunol & Med, AIDS Inst, Los Angeles, CA 90095 USA
Chen, ISY
[1
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机构:
[1] Univ Calif Los Angeles, Sch Med, Dept Microbiol & Immunol & Med, AIDS Inst, Los Angeles, CA 90095 USA
[2] Univ Calif Los Angeles, Sch Med, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90095 USA
[3] Univ Calif Los Angeles, Sch Med, Dept Med, AIDS Inst, Los Angeles, CA 90095 USA
[4] W Los Angeles Vet Affairs Med Ctr, Los Angeles, CA 90095 USA
Expression of human immunodeficiency virus-type 1 (HIV-1) Vpr after productive infection of T cells induces cell cycle arrest in the G(2) phase of the cell cycle. In the absence of de novo expression, HIV-1 Vpr packaged into virions still induced cell cycle arrest. Naturally noninfectious virus or virus rendered defective for infection by reverse transcriptase or protease inhibitors were capable of inducing Vpr-mediated cell cycle arrest. These results suggest a model whereby both infectious and noninfectious virions in vivo, such as those surrounding follicular dendritic cells, participate in immune suppression.