Taisuke Izumi

TL;DR: The current understanding of APOBEC3 structure, editing and non-editing mechanisms of AP OBEC3-mediated restriction, Vif-APOBec3 interactions that trigger APOB EC3 degradation, and the contribution of APobEC3 proteins to restriction and control of HIV-1 replication in infected patients are reviewed.

TL;DR: It is demonstrated that defective proviruses that persist in HIV-infected individuals during suppressive cART are translationally competent and produce the HIV-1 Gag and Nef proteins, which may trigger an element of innate immunity.

TL;DR: The data imply that Vif induces G2 cell cycle arrest through functional interaction with the TP53/MDM2 axis and that the G2cell cycle arrest induced by Vif has a positive effect on HIV-1 replication.

TL;DR: It is suggested that each virus has its own strategy to escape from A3 proteins and that these mechanisms might be used by other viruses that do not possess Vif-like protein.

TL;DR: The predominant accumulation of G-to-A mutations in vif-proficient HIV-1 provirus displaying characteristics of APOBEC3-mediated mutagenesis is demonstrated and provides the evidence indicating that endogenous APOBec3s are associated with G- to-A mutation of HIV- 1 provirus in vivo, which can result in the abrogation of AIDS-1 infection.