Yusuke Nakano, Hirofumi Aso, Andrew Soper, Eri Yamada, Miyu Moriwaki, Guillermo Juarez-Fernandez, Yoshio Koyanagi and Kei Sato.

Laboratory of Systems Virology, Department of Biosystems Science, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto 6068507, Japan.

Retrovirology 2017 14:31 DOI: 10.1186/s12977-017-0355-4

Apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3 (APOBEC3) proteins are mammalian-specific cellular cytidine deaminases and have a robust ability to restrain lentivirus replication. To antagonize APOBEC3-mediated antiviral action, lentiviruses have acquired viral infectivity factor (Vif) as an accessory gene. Mammalian APOBEC3 proteins inhibit lentiviral replication by enzymatically inserting G-to-A hypermutations in the viral genome, whereas lentiviral Vif proteins degrade host APOBEC3 via the ubiquitin/proteasome-dependent pathway. Recent investigations provide evidence that lentiviral vif genes evolved to combat mammalian APOBEC3 proteins. In corollary, mammalian APOBEC3 genes are under Darwinian selective pressure to escape from antagonism by Vif. Based on these observations, it is widely accepted that lentiviral Vif and mammalian APOBEC3 have co-evolved and this concept is called an “evolutionary arms race.” This review provides a comprehensive description of current knowledge with respect to the evolutionary dynamics occurring at this pivotal host-virus interface.

Figure. Dynamics of hyper/hypo HIV-1 dissemination in human population.