Department of Molecular Biology, Princeton Neuroscience Institute, Princeton University, Princeton, New Jersey 08544, USA.
Nat Rev Microbiol. 2011 Jun;9(6):427-39. doi: 10.1038/nrmicro2574. Epub 2011 Apr 27.
Viral infection converts the normal functions of a cell to optimize viral replication and virion production. One striking observation of this conversion is the reconfiguration and reorganization of cellular actin, affecting every stage of the viral life cycle, from entry through assembly to egress. The extent and degree of cytoskeletal reorganization varies among different viral infections, suggesting the evolution of myriad viral strategies. In this Review, we describe how the interaction of viral proteins with the cell modulates the structure and function of the actin cytoskeleton to initiate, sustain and spread infections. The molecular biology of such interactions continues to engage virologists in their quest to understand viral replication and informs cell biologists about the role of the cytoskeleton in the uninfected cell.
病毒感染会改变细胞的正常功能，使其优化病毒复制和病毒粒子的生成。这种转变的一个显著特征是细胞肌动蛋白的重排和重组，影响病毒生命周期的各个阶段，从进入到组装再到出芽。不同病毒感染之间细胞骨架重组的程度和范围不同，这表明病毒进化出了无数的策略。在这篇综述中，我们描述了病毒蛋白与细胞的相互作用如何调节肌动蛋白细胞骨架的结构和功能，从而启动、维持和传播感染。这些相互作用的分子生物学一直吸引着病毒学家去理解病毒复制，并让细胞生物学家了解细胞骨架在未感染细胞中的作用。
