Host restriction factor APOBEC3G (A3G) efficiently restricts Vif-deficient HIV-1 by being packaged with progeny virions and causing the G to A mutation during HIV-1 viral DNA synthesis as the progeny virus infects new cells. HIV-1 expresses Vif protein to resist the activity of A3G by mediating A3G degradation. This process requires the self-association of Vif in concert with A3G proteins, protein chaperones, and factors of the ubiquitination ma-chinery, which are potential targets to discover novel anti-HIV drugs. This review will describe compounds that have been reported so far to inhibit viral replication of HIV-1 by protecting A3G from Vif-mediated degradation.
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Thomas Jefferson Univ, Dept Med, Div Infect Dis, Ctr Human Virol, Philadelphia, PA 19107 USAThomas Jefferson Univ, Dept Med, Div Infect Dis, Ctr Human Virol, Philadelphia, PA 19107 USA
Wang, Feng-xiang
Huang, Jialing
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Thomas Jefferson Univ, Dept Med, Div Infect Dis, Ctr Human Virol, Philadelphia, PA 19107 USAThomas Jefferson Univ, Dept Med, Div Infect Dis, Ctr Human Virol, Philadelphia, PA 19107 USA
Huang, Jialing
Zhang, Hangxiang
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Thomas Jefferson Univ, Dept Emergency Med, Philadelphia, PA 19107 USAThomas Jefferson Univ, Dept Med, Div Infect Dis, Ctr Human Virol, Philadelphia, PA 19107 USA
Zhang, Hangxiang
Ma, Xinliang
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Thomas Jefferson Univ, Dept Emergency Med, Philadelphia, PA 19107 USAThomas Jefferson Univ, Dept Med, Div Infect Dis, Ctr Human Virol, Philadelphia, PA 19107 USA
Ma, Xinliang
Zhang, Hui
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Thomas Jefferson Univ, Dept Med, Div Infect Dis, Ctr Human Virol, Philadelphia, PA 19107 USAThomas Jefferson Univ, Dept Med, Div Infect Dis, Ctr Human Virol, Philadelphia, PA 19107 USA