The emerging coronavirus (CoV) pandemic is threatening the public health all over the world. Cytoskeleton is an intricate network involved in controlling cell shape, cargo transport, signal transduction, and cell division. Infection biology studies have illuminated essential roles for cytoskeleton in mediating the outcome of host‒virus interactions. In this review, we discuss the dynamic interactions between actin filaments, microtubules, intermediate filaments, and CoVs. In one round of viral life cycle, CoVs surf along filopodia on the host membrane to the entry sites, utilize specific intermediate filament protein as co-receptor to enter target cells, hijack microtubules for transportation to replication and assembly sites, and promote actin filaments polymerization to provide forces for egress. During CoV infection, disruption of host cytoskeleton homeostasis and modification state is tightly connected to pathological processes, such as defective cytokinesis, demyelinating, cilia loss, and neuron necrosis. There are increasing mechanistic studies on cytoskeleton upon CoV infection, such as viral protein‒cytoskeleton interaction, changes in the expression and post-translation modification, related signaling pathways, and incorporation with other host factors. Collectively, these insights provide new concepts for fundamental virology and the control of CoV infection.

中文翻译：

---

细胞骨架—宿主细胞中冠状病毒感染的关键

新兴的冠状病毒（CoV）大流行正在威胁全世界的公共健康。细胞骨架是一个复杂的网络，涉及控制细胞形状，货物运输，信号转导和细胞分裂。感染生物学研究阐明了细胞骨架在介导宿主病毒相互作用结果中的重要作用。在这篇综述中，我们讨论了肌动蛋白丝，微管，中间丝和冠状病毒之间的动态相互作用。在一轮病毒生命周期中，冠状病毒沿宿主膜上的丝状伪足冲浪至进入位点，利用特定的中间丝蛋白作为共受体进入靶细胞，劫持微管以运输至复制和装配位点，并促进肌动蛋白丝聚合为逃亡提供力量 在冠状病毒感染期间，宿主细胞骨架稳态和破坏状态的破坏与病理过程紧密相关，例如细胞分裂不良，脱髓鞘，纤毛丢失和神经元坏死。冠状病毒感染后细胞骨架的机制研究越来越多，例如病毒蛋白与细胞骨架的相互作用，表达的变化和翻译后修饰，相关的信号传导途径以及与其他宿主因子的结合。总而言之，这些见解为基础病毒学和CoV感染控制提供了新概念。表达的变化和翻译后修饰，相关的信号传导途径以及与其他宿主因子的结合。总而言之，这些见解为基础病毒学和CoV感染控制提供了新概念。表达的变化和翻译后修饰，相关的信号传导途径以及与其他宿主因子的结合。总而言之，这些见解为基础病毒学和CoV感染控制提供了新概念。