Jones N L, Lewis J C, Kilpatrick B A
Eur J Cell Biol. 1986 Aug;41(2):304-12.
Human cytomegalovirus (HCMV) infection causes a rapid, progressive disruption of the host cell cytoskeleton that correlates with actin depolymerization. Whole-mount (3D) electron microscopy was used to analyze the cytoskeleton of uninfected and HCMV-infected human lung fibroblast cells. Within 2 min of HCMV infection, localized areas of cytoskeletal disruption were observed. Disruption extended throughout the cytoplasm during the ensuing 45 to 90 min of infection and resulted in generalized cytoskeletal disorganization. Actin depolymerization occurred, as indicated by an increase in DNase I inhibition and alteration in the fluorescence pattern with rhodamine-conjugated phalloidin. Thus, actin appears to be the primary cytoskeletal target involved during HCMV infection. Fractionation of the virus seed inoculum showed that development of DNase I inhibitory activity in infected cells was associated only with the virus-containing fractions. Cytochalasin B treatment at early times of HCMV infection stimulated progeny virus production. This study demonstrates that rapid cytoskeletal disruption occurs during early periods of HCMV infection and indicates that actin depolymerization facilitates viral infectivity.
人巨细胞病毒（HCMV）感染会导致宿主细胞细胞骨架迅速、进行性破坏，这与肌动蛋白解聚相关。采用整装（三维）电子显微镜分析未感染和HCMV感染的人肺成纤维细胞的细胞骨架。在HCMV感染2分钟内，观察到细胞骨架破坏的局部区域。在随后45至90分钟的感染过程中，破坏扩展至整个细胞质，导致细胞骨架普遍紊乱。如脱氧核糖核酸酶I抑制作用增强以及与罗丹明偶联的鬼笔环肽荧光模式改变所示，发生了肌动蛋白解聚。因此，肌动蛋白似乎是HCMV感染期间涉及的主要细胞骨架靶点。对病毒种子接种物进行分级分离显示，感染细胞中脱氧核糖核酸酶I抑制活性的产生仅与含病毒部分有关。在HCMV感染早期用细胞松弛素B处理可刺激子代病毒产生。本研究表明，HCMV感染早期会发生快速的细胞骨架破坏，并表明肌动蛋白解聚促进病毒感染性。
