Cudmore S, Cossart P, Griffiths G, Way M
Cell Biology Programme, European Molecular Biology Laboratory, Heidelberg, Germany.
Nature. 1995 Dec 7;378(6557):636-8. doi: 10.1038/378636a0.
The role of the cytoskeleton during viral infection is poorly understood. Here we show, using a combination of mutant and drug studies, that the intracellular enveloped form of vaccinia virus is capable of inducing the formation of actin tails that are strikingly similar to those seen in Listeria, Shigella and Rickettsia infections. Analysis using video microscopy reveals that single viral particles are propelled in vivo on the tip of actin tails, at a speed of 2.8 mumol min-1. On contact with the cell surface, virus particles extend outwards on actin projections at a similar rate, to contact and infect neighboring cells. Given the similarities between the motility of vaccinia virus and bacterial pathogens, we suggest that intracellular pathogens have developed a common mechanism to exploit the actin cytoskeleton as a means to facilitate their direct spread between cells.
细胞骨架在病毒感染过程中的作用尚不清楚。在此我们通过突变体和药物研究相结合的方法表明,痘苗病毒的细胞内包膜形式能够诱导肌动蛋白尾的形成,这些肌动蛋白尾与在李斯特菌、志贺氏菌和立克次氏体感染中所见的极为相似。利用视频显微镜分析发现,单个病毒颗粒在肌动蛋白尾的尖端以2.8微米/分钟的速度在体内推进。与细胞表面接触时,病毒颗粒以相似的速度在肌动蛋白突起上向外延伸,以接触并感染邻近细胞。鉴于痘苗病毒和细菌病原体运动性之间的相似性,我们认为细胞内病原体已经形成了一种共同机制,利用肌动蛋白细胞骨架作为促进它们在细胞间直接传播的手段。