Antagonistic Effect of Virion Infectivity Factor and APOBEC3G in the Intrinsic Antiretroviral Defense

Abstract: The virion infectivity factor (Vif) is one of the six human immunodeficiency virus (HIV) accessory proteins. It is essential for efficient viral replication. For a long time， the progress in Vif function is limited because the complexity of its function and correspondingly complex systems are not clear. Until 2002， some studies have revealed the apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3G (APOBEC3G) is a potent intrinsic inhibitor of retroviral replication. Vif function has been rapidly elucidated. APOBEC3G blocks the productive infection of HIV-1 mainly through cytidine deaminase activity. APOBEC3G effectively halts HIV replication by lethal dC to dU editing and dG to dA hypermutation during the reverse transcription. Retroviruses have evolved Vif to counter the antiretroviral action of APOBEC3G. Firstly， Vif can directly induce APOBEC3G rapid degradation via the ubiquitin-proteasomal pathway. Secondly， Vif inhibits the translation of APOBEC3G mRNA， further reducing the enzyme within the cell. In addition， Vif might promote the transition of APOBEC3G from low molecular mass (LMM) to high molecular mass (HMM) conformations， thereby defeats the antiviral activity of APOBEC3G. The further research on the reaction of Vif/APOBEC3G will provide the theoretical basis for the antiviral drug development.
    

CSTR: 32200.14.cjcb.2008.03.0004