Several members of the APOBEC3 family of cellular restriction factors provide 
intrinsic immunity to the host against viral infection. Specifically, APOBEC3DE, 
APOBEC3F, APOBEC3G, and APOBEC3H haplotypes II, V, and VII provide protection 
against HIV-1Δvif through hypermutation of the viral genome, inhibition of 
reverse transcription, and inhibition of viral DNA integration into the host 
genome. HIV-1 counteracts APOBEC3 proteins by encoding the viral protein Vif, 
which contains distinct domains that specifically interact with these APOBEC3 
proteins to ensure their proteasomal degradation, allowing virus replication to 
proceed. Here, we review our current understanding of APOBEC3 structure, editing 
and non-editing mechanisms of APOBEC3-mediated restriction, Vif-APOBEC3 
interactions that trigger APOBEC3 degradation, and the contribution of APOBEC3 
proteins to restriction and control of HIV-1 replication in infected patients.