Abstract
The viral infectivity factor gene (vif) of HIV-1 increases the infectivity of viral particles by inactivation of cellular anti-viral factors, and supports productive viral replication in primary human CD4 T cells and in certain non-permissive T cell lines. Here, we demonstrate that Vif also contributes to the arrest of HIV-1 infected cells in the G2 phase of the cell cycle. Viruses deleted in Vif or Vpr induce less cell cycle arrest than wild-type virus, while cells infected with HIV-1 deleted in both Vif and Vpr have a cell cycle profile equivalent to that of uninfected cells. Furthermore, expression of Vif alone induces accumulation of cells in the G2 phase of the cell cycle. These data demonstrate a novel role for Vif in cell cycle regulation and suggest that Vif and Vpr independently drive G2 arrest in HIV-1 infected cells. Our results may have implications for the actions and interactions of key HIV-1 accessory proteins in AIDS pathogenesis.
Original language | English (US) |
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Pages (from-to) | 243-252 |
Number of pages | 10 |
Journal | Virology |
Volume | 359 |
Issue number | 2 |
DOIs | |
State | Published - Mar 15 2007 |
Externally published | Yes |
Keywords
- Cell cycle
- HIV-1 accessory proteins
- T cells
- Vif
- Vpr
ASJC Scopus subject areas
- Virology