Induction of APOBEC3G Ubiquitination and Degradation by an HIV-1 Vif-Cul5-SCF Complex

Xianghui Yu, Yunkai Yu, Bindong Liu, Kun Luo, Wei Kong, Panyong Mao, Xiao Fang Yu

Research output: Contribution to journalArticlepeer-review

951 Scopus citations


Human immunodeficiency virus-1 (HIV-1) Vif is essential for viral evasion of host antiviral factor CEM15/APOBEC3G. We report that Vif interacts with cellular proteins Cul5, elongins B and C, and Rbx1 to form an Skp1-cullin-F-box (SCF)-like complex. The ability of Vif to suppress antiviral activity of APOBEC3G was specifically dependent on Cul5-SCF function, allowing Vif to interact with APOBEC3G and induce its ubiquitination and degradation. A Vif mutant that interacted with APOBEC3G but not with Cul5-SCF was functionally inactive. The Cul5-SCF was also required for Vif function in distantly related simian immunodeficiency virus mac. These results indicate that the conserved Cul5-SCF pathway used by Vif is a potential target for antiviral development.

Original languageEnglish (US)
Pages (from-to)1056-1060
Number of pages5
Issue number5647
StatePublished - Nov 7 2003

ASJC Scopus subject areas

  • General


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