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Lentiviruses, a subfamily of retroviruses, cause slow infec-tions in humans and animals. Human immunodeficiency virus type 1 (HIV-1), simian immunodeficiency virus (SIV), caprine arthritis-encephalitis virus (CAEV), fe-line immunodeficiency virus (FIV), bovine immunodefi-ciency virus (BIV), maedi-visna virus (MVV) and equine infectious anemia virus (EIAV) are lentiviruses that infect humans, monkeys, goats, cats, cattle, sheep and horses, respectively. Except for EIAV, all lentiviruses require the accessory protein viral infectivity factor (Vif) to establish persistent infection and pathogenesis in vivo [1]. The Vif protein counteracts the antiviral activities of the apolipo-protein B mRNA-editing enzyme, catalytic polypeptide-like 3 (APOBEC3 or A3) proteins of the host [2]. These A3 proteins possess broad antiviral activities for many vi-ruses as natural host restriction factors [3-7]. Among the A3 proteins, A3G is the most intensively studied. In the late stage of viral infection, A3G proteins are packaged into virions and induce dC to dU mutations in newly syn-thesized minus-strand viral DNA. These mutations cause abnormal expression of viral proteins, resulting in disrup