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

Blood | Jan 27, 2011

http://www.ncbi.nlm.nih.gov/pubmed/21149631

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 RIS Download

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

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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

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