The viral infectivity factor (Vif) of HIV type-1 (HIV-1) is essential for efficient viral replication, yet was, until recently, enigmatic. This resulted from the complexity and cellular specificity of its function and the correspondingly complex systems that are required for its investigation. These limitations have been overcome and Vif function has been rapidly elucidated, with implications for the development of drugs to block its activity. These studies have revealed a novel component of the innate immune system, APOBEC3G, that lethally hypermutates retroviruses, including HIV-1. For HIV-1, the competition between the virus and APOBEC3G is tipped in favor of the invader by Vif, which binds to APOBEC3G and triggers its polyubiquitination and rapid degradation, thereby preventing its entry into progeny virions.
机构:
Univ Miami, Miller Sch Med, Div Infect Dis, Miami, FL 33136 USAUniv Massachusetts, Sch Med, Chem Biol Program, Dept Biochem & Mol Pharmacol, Worcester, MA 01605 USA
Sharova, Natalia
Stevenson, Mario
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Univ Miami, Miller Sch Med, Div Infect Dis, Miami, FL 33136 USAUniv Massachusetts, Sch Med, Chem Biol Program, Dept Biochem & Mol Pharmacol, Worcester, MA 01605 USA
Stevenson, Mario
Rana, Tariq M.
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Univ Massachusetts, Sch Med, Chem Biol Program, Dept Biochem & Mol Pharmacol, Worcester, MA 01605 USA
Sanford Burnham Med Res Inst, Program RNA Biol, La Jolla, CA 92037 USAUniv Massachusetts, Sch Med, Chem Biol Program, Dept Biochem & Mol Pharmacol, Worcester, MA 01605 USA
机构:
Thomas Jefferson Univ, Jefferson Med Coll, Dept Med,Dorrance Hamilton Labs, Div Infect Dis & Environm Med,Ctr Human Virol & B, Philadelphia, PA 19107 USAThomas Jefferson Univ, Jefferson Med Coll, Dept Med,Dorrance Hamilton Labs, Div Infect Dis & Environm Med,Ctr Human Virol & B, Philadelphia, PA 19107 USA