Department of Microbiology and Molecular Medicine, Faculty of Medicine University of Geneva, CMU, 1 rue Michel-Servet, 1211 Geneva 4, Switzerland.
Virology. 2011 Feb 5;410(1):7-16. doi: 10.1016/j.virol.2010.10.003. Epub 2010 Nov 13.
Cytoplasmic actins have been found interacting with viral proteins and identified in virus particles. We analyzed by confocal microscopy the cytoplasmic β- and γ-actin patterns during the course of Sendai virus infections in polarized cells. We observed a spectacular remodeling of the β-cytoplasmic actin which correlated with productive viral multiplication. Conversely, suppression of M during the course of a productive infection resulted in the decrease of particle production and the absence of β-actin remodeling. As concomitant suppression of β- and γ-actins resulted as well in reduction of virus particle production, we propose that Sendai virus specifically induces actin remodeling in order to promote efficient virion production. Beta- and γ-cytoplasmic actin recruitment could substitute for that of the endosomal sorting complex required for transport (ESCRT) mobilized by other enveloped viruses but apparently not used by Sendai virus.
细胞质肌动蛋白已被发现与病毒蛋白相互作用,并在病毒颗粒中被鉴定。我们通过共聚焦显微镜分析了在极化细胞中仙台病毒感染过程中细胞质β-和γ-肌动蛋白的模式。我们观察到β-细胞质肌动蛋白的惊人重塑,这与病毒的有效增殖相关。相反,在有效的感染过程中抑制 M 会导致颗粒产生减少和β-肌动蛋白重塑缺失。由于同时抑制β-和γ-肌动蛋白也会导致病毒颗粒产生减少,因此我们提出仙台病毒特异性诱导肌动蛋白重塑,以促进有效的病毒粒子产生。β-和γ-细胞质肌动蛋白的募集可以替代其他包膜病毒通过内体分选复合物所必需的肌动蛋白募集(ESCRT),但显然不是仙台病毒所利用的。