Abstract
Expression of human immunodeficiency virus-type 1 (HIV-1) Vpr after productive infection of T cells induces cell cycle arrest in the G2 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.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Anti-HIV Agents / pharmacology
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G2 Phase* / drug effects
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Gene Products, vpr / physiology*
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Genes, Reporter
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Genes, vpr
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HIV Protease Inhibitors / pharmacology
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HIV-1 / drug effects
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HIV-1 / physiology*
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HeLa Cells
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Humans
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Indinavir / pharmacology
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Leukocytes / virology
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Nevirapine / pharmacology
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Reverse Transcriptase Inhibitors / pharmacology
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Thy-1 Antigens / analysis
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Thy-1 Antigens / genetics
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Virion / physiology
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Zidovudine / pharmacology
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vpr Gene Products, Human Immunodeficiency Virus
Substances
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Anti-HIV Agents
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Gene Products, vpr
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HIV Protease Inhibitors
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Reverse Transcriptase Inhibitors
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Thy-1 Antigens
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vpr Gene Products, Human Immunodeficiency Virus
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Zidovudine
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Indinavir
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Nevirapine