Sakuma Ryuta, Takeuchi Hiroaki
Department of Molecular Virology, Tokyo Medical and Dental University, Tokyo, Japan.
Front Microbiol. 2012 Apr 27;3:162. doi: 10.3389/fmicb.2012.00162. eCollection 2012.
Current human immunodeficiency virus type 1 pandemic is believed to originate from cross-species transmission of simian immunodeficiency virus (SIV) into human population. Such cross-species transmission, however, is not efficient in general, because viral replication is modulated by host cell factors, with the species-specificity of these factors affecting viral tropism. An understanding of those host cell factors that affect viral replication contributes to elucidation of the mechanism for determination of viral tropism. This review will focus an anti-viral effect of ApoB mRNA editing catalytic subunit, tripartite motif protein 5 alpha, and cyclophilins on SIV replication and provide insight into the mechanism of species-specific barriers against viral infection in human cells. It will then present our current understanding of the mechanism that may explain zoonotic transmission of retroviruses.
目前认为，1型人类免疫缺陷病毒的全球大流行源于猿猴免疫缺陷病毒（SIV）跨物种传播至人类群体。然而，这种跨物种传播通常效率不高，因为病毒复制受宿主细胞因子调控，这些因子的物种特异性影响病毒嗜性。了解那些影响病毒复制的宿主细胞因子有助于阐明病毒嗜性的决定机制。本综述将聚焦载脂蛋白B信使核糖核酸编辑催化亚基、三联基序蛋白5α和亲环蛋白对SIV复制的抗病毒作用，并深入探讨人类细胞中针对病毒感染的物种特异性屏障机制。随后，本文将阐述我们目前对可能解释逆转录病毒人畜共患传播机制的理解。
