The Vif Accessory Protein Alters the Cell Cycle of Human Immunodeficiency Virus Type 1 Infected Cells (45.15)

• Published in: The Journal of immunology (1950) Vol. 178; no. 1_Supplement; p. S60
• Main Authors: Wang, Jiangfang, Shackelford, Jason M., Casella, Carolyn R., Shivers, Debra K., Rapaport, Eric L., Liu, Bindong, Yu, Xiao-Fang, Finkel, Terri H.
• Format: Journal Article
• Language: English
• Published: 01.04.2007
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.178.Supp.45.15

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.