Fackler Oliver T, Kräusslich Hans-Georg
Department of Virology, University of Heidelberg, Im Neuenheimer Feld 324, D-69120 Heidelberg, Germany.
Curr Opin Microbiol. 2006 Aug;9(4):409-15. doi: 10.1016/j.mib.2006.06.010. Epub 2006 Jul 3.
As obligate cell parasites, viruses have evolved into professional manipulators of host cell functions. Accordingly, viruses often remodel the cytoskeleton of target cells in order to convert one of the cell's barriers to viral replication into a vehicle for the virus that facilitates the generation of infectious progeny. Surprisingly little is known about the mechanisms employed by two major human pathogens, HIV and human T-cell leukaemia virus (HTLV), to exploit host cell cytoskeletal dynamics. New studies have begun to unravel how these retroviruses remodel cytoskeletal structures to facilitate entry into, transport within and egress from target cells. Exciting progress has been made in understanding how HIV and HTLV polarize actin and also control microtubule organization to spread from donor to target cells in close cell-contacts termed virological synapses.
作为专性细胞内寄生生物,病毒已进化成为宿主细胞功能的专业操纵者。因此,病毒常常重塑靶细胞的细胞骨架,以便将细胞对病毒复制的一种屏障转化为病毒的载体,促进感染性子代病毒的产生。令人惊讶的是,对于两种主要的人类病原体——人类免疫缺陷病毒(HIV)和人类T细胞白血病病毒(HTLV)——利用宿主细胞细胞骨架动力学的机制,我们知之甚少。新的研究已开始揭示这些逆转录病毒如何重塑细胞骨架结构,以促进其进入靶细胞、在靶细胞内运输以及从靶细胞中释放。在理解HIV和HTLV如何极化肌动蛋白以及控制微管组织以在称为病毒突触的紧密细胞接触中从供体细胞传播到靶细胞方面,已取得了令人兴奋的进展。