Background:  Over the past few years several host proteins with potent anti-viral activity have been detailed. In particular, the APOBEC3F and APOBEC3G proteins can strongly block the replication of Vif-defective HIV-1. Much of this inhibitory activity is manifested through the deamination of viral cDNA cytosines to uracils during reverse transcription. However, this rarely occurs in vivo because the viral accessory protein Vif effectively neutralizes these APOBEC3 proteins. Vif is therefore required for virus replication.

Conclusions:  Strategies to modulate this delicate balance and thereby protect these host APOBEC3 proteins from Vif will be discussed.