Jeffree Chris E, Brown Gaie, Aitken Jim, Su-Yin Dawn Yeo, Tan Boon-Huan, Sugrue Richard J
School of Biological Sciences, Daniel Rutherford Building, King's Buildings, Mayfield Road, University of Edinburgh Edinburgh, EH9 3JH, UK.
Virology. 2007 Dec 20;369(2):309-23. doi: 10.1016/j.virol.2007.08.007. Epub 2007 Sep 6.
During respiratory syncytial virus (RSV) infection there is a close physical interaction between the filamentous actin (F-actin) and the virus, involving both inclusion bodies and the virus filaments. This interaction appears to occur relatively early in the replication cycle, and can be detected from 8 h post-infection. Furthermore, during virus assembly we obtained evidence for the participation of an F-actin-associated signalling pathway involving phosphatidyl-3-kinase (PI3K). Treatment with the PI3K inhibitor LY294002 prevented the formation of virus filaments, although no effect was observed either on virus protein expression, or on trafficking of the virus glycoproteins to the cell surface. Inhibition of the activity of Rac GTPase, a down-stream effector of PI3K, by treatment with the Rac-specific inhibitor NSC23766 gave similar results. These data suggest that an intimate interaction occurs between actin and RSV, and that actin-associated signalling pathway, involving PI3K and Rac GTPase, may play an important role during virus assembly.
在呼吸道合胞病毒（RSV）感染期间，丝状肌动蛋白（F-肌动蛋白）与病毒之间存在密切的物理相互作用，这涉及包涵体和病毒丝。这种相互作用似乎在复制周期中相对较早发生，并且在感染后8小时即可检测到。此外，在病毒组装过程中，我们获得了涉及磷脂酰-3-激酶（PI3K）的F-肌动蛋白相关信号通路参与的证据。用PI3K抑制剂LY294002处理可阻止病毒丝的形成，尽管对病毒蛋白表达或病毒糖蛋白向细胞表面的转运均未观察到影响。用Rac特异性抑制剂NSC23766处理抑制PI3K的下游效应器Rac GTPase的活性，得到了类似的结果。这些数据表明肌动蛋白与RSV之间存在密切的相互作用，并且涉及PI3K和Rac GTPase的肌动蛋白相关信号通路可能在病毒组装过程中起重要作用。
