Perez Omar, Hope Thomas J
Department of Cell and Molecular Biology, Northwestern University, 303 East Chicago Avenue, Chicago, Illinois 60611-3008, USA.
Curr HIV/AIDS Rep. 2006 Feb;3(1):20-5. doi: 10.1007/s11904-006-0004-3.
Several innate immune mechanisms exist in mammalian cells that prevent the replication of viruses. These cellular factors influence the tropism of retroviruses in mammalian cells by inducing a dominant restriction that acts after viral entry but before integration into the host genome. The identification of several cellular factors involved with the post entry block of HIV has recently been revealed. These recent advances identified the tripartite motif protein 5alpha (Trim5alpha) and the apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3G (APOBEC3G), which work to inactivate several retroviruses including HIV-1. The mechanism of restriction by these cellular proteins is unknown. Therefore, this review highlights recent advances in understanding the function of Trim5alpha and APOBEC3G.
哺乳动物细胞中存在多种先天性免疫机制来阻止病毒复制。这些细胞因子通过诱导一种显性限制来影响逆转录病毒在哺乳动物细胞中的嗜性，这种限制作用于病毒进入细胞后但在整合到宿主基因组之前。最近已经揭示了几种与HIV进入后阻断相关的细胞因子。这些最新进展确定了三联基序蛋白5α（Trim5α）和载脂蛋白B mRNA编辑酶催化多肽样3G（APOBEC3G），它们可使包括HIV-1在内的多种逆转录病毒失活。这些细胞蛋白的限制机制尚不清楚。因此，本综述重点介绍了在理解Trim5α和APOBEC3G功能方面的最新进展。
