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HIV-1 Vif promotes the G₁- to S-phase cell-cycle transition.

HIV-1 depends on host-cell resources for replication, access to which may be limited to a particular phase of the cell cycle. The HIV-encoded proteins Vpr (viral protein R) and Vif (viral infectivity factor) arrest cells in the G₂ phase; however, alteration of other cell-cycle phases has not been reported. We show that Vif drives cells out of G₁ and into the S phase. The effect of Vif on the G₁- to-S transition is distinct from its effect on G₂, because G₂ arrest is Cullin5-dependent, whereas the G₁- to-S progression is Cullin5-independent. Using mass spectrometry, we identified 2 novel cellular partners of Vif, Brd4 and Cdk9, both of which are known to regulate cell-cycle progression. We confirmed the interaction of Vif and Cdk9 by immunoprecipitation and Western blot, and showed that small interfering RNAs (siRNAs) specific for Cdk9 inhibit the Vif-mediated G₁- to-S transition. These data suggest that Vif regulates early cell-cycle progression, with implications for infection and latency.

Pubmed ID: 21149631


  • Wang J
  • Reuschel EL
  • Shackelford JM
  • Jeang L
  • Shivers DK
  • Diehl JA
  • Yu XF
  • Finkel TH



Publication Data

January 27, 2011

Associated Grants

  • Agency: NIAID NIH HHS, Id: 1T32 AI007632
  • Agency: NIAID NIH HHS, Id: R01 AI062644
  • Agency: NIAID NIH HHS, Id: R01 AI062644
  • Agency: NIAID NIH HHS, Id: R01 AI062644-05
  • Agency: NIAID NIH HHS, Id: R01 AI35513
  • Agency: NIAID NIH HHS, Id: R01 AI40003
  • Agency: NCI NIH HHS, Id: R01 CA093237

Mesh Terms

  • Cell Cycle
  • Cell Proliferation
  • Cullin Proteins
  • Cyclin-Dependent Kinase 9
  • G1 Phase
  • Gene Expression Regulation
  • HIV Infections
  • HIV-1
  • HeLa Cells
  • Humans
  • Models, Biological
  • Mutant Proteins
  • Protein Binding
  • RNA, Small Interfering
  • S Phase
  • Transfection
  • Virus Latency
  • vif Gene Products, Human Immunodeficiency Virus