Ehrlich Elana S, Yu Xiao-Fang
Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland 21205, USA.
Int J Hematol. 2006 Apr;83(3):208-12. doi: 10.1532/IJH97.06013.
Since the beginning of time, microorganisms have been devising ways to bypass detection and destruction by our immune system. Therefore, it is no surprise that along with the identification of the cellular antiviral protein APOBEC3G (A3G) has come the recognition of the viral solution to this assault. Here, we review the research that led up to the identification of A3G and the mechanism that the human immunodeficiency virus protein Vif developed to evade A3G's antiviral activities.
从一开始,微生物就一直在想方设法避开我们免疫系统的检测和破坏。因此,随着细胞抗病毒蛋白载脂蛋白B mRNA编辑酶催化多肽样蛋白3G(APOBEC3G,A3G)的发现,人们认识到病毒针对这种攻击的应对办法也就不足为奇了。在此,我们回顾了促成A3G发现的相关研究,以及人类免疫缺陷病毒蛋白Vif为逃避A3G的抗病毒活性而形成的机制。