in HIV-1 Replication

Abstract

Vif is required for HIV-1 replication in primary cells and other nonpermissive cell lines. The function of Vif was unknown until recent papers revealed that it prevents the encapsidation of APOBEC3G and APOBEC3F, two potent antiretroviral cytidine deaminases. APOBEC3G and APOBEC3F inhibit the replication of ∆vif HIV-1 by deaminating the minus-strand of the viral reverse transcripts, introducing numerous G→A mutations. These two APOBEC3 family members appear to be the major contributors to G→A hypermutation in HIV-1 in vivo. Here we review recent advances in the field, emphasizing the sequence specificity of the antiviral APOBEC3 deaminases and their roles in molding the viral genome.