Cell cycle arrest by Vpr in HIV-1 virions and insensitivity to antiretroviral agents

Science. 1998 Jul 10;281(5374):266-9. doi: 10.1126/science.281.5374.266.

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

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Anti-HIV Agents / pharmacology
  • G2 Phase* / drug effects
  • Gene Products, vpr / physiology*
  • Genes, Reporter
  • Genes, vpr
  • HIV Protease Inhibitors / pharmacology
  • HIV-1 / drug effects
  • HIV-1 / physiology*
  • HeLa Cells
  • Humans
  • Indinavir / pharmacology
  • Leukocytes / virology
  • Nevirapine / pharmacology
  • Reverse Transcriptase Inhibitors / pharmacology
  • Thy-1 Antigens / analysis
  • Thy-1 Antigens / genetics
  • Virion / physiology
  • Zidovudine / pharmacology
  • vpr Gene Products, Human Immunodeficiency Virus

Substances

  • Anti-HIV Agents
  • Gene Products, vpr
  • HIV Protease Inhibitors
  • Reverse Transcriptase Inhibitors
  • Thy-1 Antigens
  • vpr Gene Products, Human Immunodeficiency Virus
  • Zidovudine
  • Indinavir
  • Nevirapine