APOBEC3G is a member of a family of enzymes that have potent DNA mutator activity. APOBEC3G deaminates deoxycytosine to deoxyuracil in the minus strand of HIV-1 DNA, resulting in G to A hypermutation in the plus strand of DNA. Thus, APOBEC3G provides a mechanism for innate immunity to retroviruses and also likely contributes to sequence variation observed in many viruses. Viral infectivity factor (Vif) imparts APOBEC3G resistance to HIV through impaired translation of APOBEC3G mRNA and accel-erated posttranslational degradation of APOBEC3G by the 26S proteasome. Inter-estingly, HIV-1 Vif cannot form a complex with APOBEC3G of mouse origin as it does with the human protein, and thus mouse APOBEC3G functions as a potent inhibitor of wild type HIV-1 replication, where human APOBEC3G is only able to inhibit Vif-deficient HIV-1 replication. This implies that induction of APOBEC3G activity or a method of blocking its interaction with Vif may provide a method for therapeutic intervention. CEM15 is a 429 amino acid mouse protein that is thought to function as an ortholog of human APOBEC3G.