肌动蛋白依赖的运动能力丧失会损害体外的水疱性口炎病毒释放，但对体内传播并不关键。
Loss of Actin-Based Motility Impairs Ectromelia Virus Release In Vitro but Is Not Critical to Spread In Vivo.
机构信息
School of Life and Environmental Sciences, The University of Sydney, Sydney, NSW 2006, Australia.
School of Medicine, College of Health and Medicine, The University of Tasmania, Hobart, TAS 7005, Australia.
出版信息
Viruses. 2018 Mar 5;10(3):111. doi: 10.3390/v10030111.
Ectromelia virus (ECTV) is an orthopoxvirus and the causative agent of mousepox. Like other poxviruses such as variola virus (agent of smallpox), monkeypox virus and vaccinia virus (the live vaccine for smallpox), ECTV promotes actin-nucleation at the surface of infected cells during virus release. Homologs of the viral protein A36 mediate this function through phosphorylation of one or two tyrosine residues that ultimately recruit the cellular Arp2/3 actin-nucleating complex. A36 also functions in the intracellular trafficking of virus mediated by kinesin-1. Here, we describe the generation of a recombinant ECTV that is specifically disrupted in actin-based motility allowing us to examine the role of this transport step in vivo for the first time. We show that actin-based motility has a critical role in promoting the release of virus from infected cells in vitro but plays a minor role in virus spread in vivo. It is likely that loss of microtubule-dependent transport is a major factor for the attenuation observed when is deleted.
细小病毒（ECTV）是一种正痘病毒，也是小鼠痘的病原体。像其他痘病毒，如天花病毒（引起天花的病原体）、猴痘病毒和牛痘病毒（天花的活疫苗）一样，细小病毒在病毒释放过程中促进感染细胞表面的肌动蛋白成核。病毒蛋白 A36 的同源物通过一个或两个酪氨酸残基的磷酸化来介导此功能，最终招募细胞的 Arp2/3 肌动蛋白成核复合物。A36 还在由驱动蛋白-1 介导的病毒细胞内运输中发挥作用。在这里，我们描述了一种重组细小病毒的产生，该病毒在肌动蛋白依赖性运动方面特异性缺失，使我们能够首次在体内研究这一运输步骤的作用。我们表明，肌动蛋白依赖性运动在促进感染细胞中病毒的释放方面起着关键作用，但在体内病毒传播中作用较小。当 缺失时，观察到的减毒可能主要是由于微管依赖性运输的丧失所致。
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