Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA; email:
Department of Chemistry, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA.
Annu Rev Virol. 2020 Sep 29;7(1):167-187. doi: 10.1146/annurev-virology-010320-070410. Epub 2020 May 26.
Influenza virus exploits cellular factors to complete each step of viral replication. Yet, multiple host proteins actively block replication. Consequently, infection success depends on the relative speed and efficacy at which both the virus and host use their respective effectors. Post-translational modifications (PTMs) afford both the virus and the host means to readily adapt protein function without the need for new protein production. Here we use influenza virus to address concepts common to all viruses, reviewing how PTMs facilitate and thwart each step of the replication cycle. We also discuss advancements in proteomic methods that better characterize PTMs. Although some effectors and PTMs have clear pro- or antiviral functions, PTMs generally play regulatory roles to tune protein functions, levels, and localization. Synthesis of our current understanding reveals complex regulatory schemes where the effects of PTMs are time and context dependent as the virus and host battle to control infection.
流感病毒利用细胞因子完成病毒复制的每一个步骤。然而,许多宿主蛋白积极地阻断复制。因此,感染的成功取决于病毒和宿主各自利用其效应子的相对速度和效率。翻译后修饰(PTMs)为病毒和宿主提供了一种无需新蛋白产生即可快速适应蛋白功能的手段。在这里,我们使用流感病毒来解决所有病毒共有的概念,回顾 PTMs 如何促进和阻碍复制周期的每一步。我们还讨论了更好地表征 PTMs 的蛋白质组学方法的进展。尽管一些效应物和 PTMs 具有明确的促病毒或抗病毒功能,但 PTMs 通常发挥调节作用,以调整蛋白功能、水平和定位。对我们目前理解的综合分析揭示了复杂的调控方案,其中 PTMs 的影响是时间和上下文依赖的,因为病毒和宿主在控制感染方面进行斗争。