Interestingly, throughout evolution, the retroviruses of many mammals appear to have become largely immune to APOBEC3G or to the APOBEC3G-like proteins of their hosts. HIV-1 expresses an accessory protein, Vif, which neutralizes APOBEC3G through ubiquitination and degradation [33] [34] [35] [36] . Simian immunodeficiency virus (SIV) uses a similar Vif-dependent mechanism [17, 26] . Foamy viruses employ an unrelated viral protein called Bet, for which the precise neutralization mechanism is currently unclear [37, 38] . Murine leukaemia virus (MLV) and human T-lymphotrophic virus-1 (HTLV-1) may simply avoid APOBEC3 proteins by preventing encapsidation [26, 39, 40] .