详细记录  
题名:Murine Retrovirus Escapes from Murine APOBEC3 via Two Distinct Novel Mechanisms
作者:Aierken Abudu, Akifumi Takaori-Kondo,...
来源:Current Biology 2006 16: 1565-1570.
URL :http://dx.doi.org/10.1016/j.cub.2006.06.055
日期:061215
摘要:Aierken Abudu1, Akifumi Takaori-Kondo1, , , Taisuke Izumi1, Kotaro Shirakawa1, Masayuki Kobayashi1, Amane Sasada1, Keiko Fukunaga1 and Takashi Uchiyama1

1Department of Hematology and Oncology, Graduate School of Medicine, Kyoto University, 54 Shogoin-Kawaracho, Sakyo-ku, Kyoto 606-8507, Japan


Summary

APOBEC3G (A3G) is an antiretroviral host factor that functions by deaminating dC to dU in retroviral cDNA 1, 2, 3, 4 and 5. HIV-1 Vif protein counteracts A3G via a ubiquitin-proteasome pathway 6, 7, 8, 9, 10, 11 and 12. In the case of a simple retrovirus such as the murine leukemia virus (MLV), it remains unclear why it can replicate in cells expressing APOBEC3 (A3) even though it doesn`t possess any accessory proteins such as Vif 2 and 13. In this study, we demonstrate that MLV escapes from murine A3 (mA3) via two distinct novel mechanisms. First, viral RNA (vRNA) blocks the binding of mA3 to Gag, resulting in the exclusion of mA3 from MLV virions. Second, viral protease (vPR) cleaves mA3 after maturation of virions. Here, we suggest 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. On the other hand, mice possess another form of mA3, Δexon5, that escapes from the cleavage by vPR to show more antiviral activity than the wild type mA3. This also suggests that battles between host intrinsic immunity and viruses have led to the evolution of proteins on both sides.

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