Chiang Karen, Rice Andrew P
Interdepartmental Program in Translational Biology & Molecular Medicine, Baylor College of Medicine, TX, USA.
Future Virol. 2011 Feb;6(2):209-221. doi: 10.2217/fvl.10.92.
Cellular restriction of HIV-1 replication has traditionally been thought of as protein mediated: APOBEC3G hypermutates HIV-1 genomic RNA, but is counteracted by Vif; Tetherin inhibits the release of budding virions but is counteracted by Vpu. In recent years, new evidence suggesting that miRNAs and other components of the miRNA pathway act as HIV-1 restriction factors has come to light, along with the identification of strategies that HIV-1 employs to surmount these host obstacles. In this article, we summarize and discuss the literature to date regarding the complex relationship between HIV-1 and miRNA-mediated inhibition.
传统上，人们认为HIV-1复制的细胞限制是由蛋白质介导的：载脂蛋白B mRNA编辑酶催化多肽样蛋白3G（APOBEC3G）使HIV-1基因组RNA发生高度突变，但可被Vif蛋白抵消；束缚蛋白抑制出芽病毒粒子的释放，但可被Vpu蛋白抵消。近年来，新的证据表明，微小RNA（miRNA）和miRNA途径的其他成分可作为HIV-1限制因子，同时也发现了HIV-1克服这些宿主障碍所采用的策略。在本文中，我们总结并讨论了迄今为止关于HIV-1与miRNA介导的抑制之间复杂关系的文献。
