Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

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