Suhasini Modem, Reddy Thipparthi R
Department of Immunology & Microbiology, Wayne State University, Detroit, MI, USA.
Curr HIV Res. 2009 Jan;7(1):91-100. doi: 10.2174/157016209787048474.
The human immunodeficiency virus (HIV-1) differentially controls viral protein expression at the level of splicing as well as nuclear export of incompletely spliced viral RNA. This process, mediated by the Rev protein, interfaces with cellular components involved in post-transcriptional gene regulation. While a number of reviews have focused on the host proteins (i.e., Crm1, importin-beta and nucleoporins) that specifically regulate shuttling of Rev between the nucleus and cytoplasm, we could find no systematic review of other cellular proteins implicated in Rev function. Therefore, we will here focus on other Rev cofactors (eIF5a, hRIP, Sam68, RNA helicases, etc) and the role they play in Rev/RRE function and HIV-1 replication.
人类免疫缺陷病毒1型（HIV-1）在剪接水平以及不完全剪接的病毒RNA的核输出方面对病毒蛋白表达进行差异控制。这一过程由Rev蛋白介导，与参与转录后基因调控的细胞成分相互作用。虽然已有许多综述聚焦于特异性调节Rev在细胞核与细胞质之间穿梭的宿主蛋白（即Crm1、输入蛋白β和核孔蛋白），但我们未找到对其他与Rev功能相关的细胞蛋白的系统综述。因此，我们将在此聚焦于其他Rev辅助因子（eIF5a、hRIP、Sam68、RNA解旋酶等）以及它们在Rev/RRE功能和HIV-1复制中所起的作用。
