are viruses inhibited by apobec3 molecules from their host species由apobec3病毒抑制宿主物种的分子.pdfVIP

Opinion Are Viruses Inhibited by APOBEC3 Molecules from Their Host Species? Susan R. Ross* Department of Microbiology and Abramson Family Cancer Center, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America Organisms adapt to infectious agents by factor (Vif) [5]. hA3G and subsequently resistant to the A3 proteins of their natural developing protective responses, and con- hA3F were shown to inhibit HIV-1 lacking hosts. For example, it has been shown that versely, infectious agents develop adaptive the vif gene. In vif-deficient HIV-1 pro- human T cell leukemia virus I (HTLVI), countermeasures to these responses. Host ducer cells, both hA3G and hA3F are Mason Pfizer monkey virus (MPMV), and defenses against infectious agents include packaged into progeny virions via interac- MLV do not efficiently package human, adaptive and innate immune responses tion with the nucleocapsid (NC) protein monkey, or mouse A3 proteins, respec- (e.g., natural killer cells, Toll-like recep- and viral RNA. Once packaged, hA3 tively, because of weak interactions be- tors, and interferons). Recently, additional proteins inhibit infection in target cells by tween the NC proteins and the host A3 host defense systems against viruses have deaminating deoxycytidine residues on the [38–46], although other studies have been identified. These include the TRIM DNA minus strand following reverse shown some packaging of host A3 proteins [1], RIGI/MDA5 [2], Bst2/tetherin [3,4], transcription, inducing G to A hypermuta- by HTLVI and MLV as well as viral and APOBEC3 (A3) [5] proteins. Many of