Gatti Priya, Ilamathi Hema Saranya, Todkar Kiran, Germain Marc
Groupe de Recherche en Signalisation Cellulaire and Département de Biologie, Médicale, Université du Québec à Trois-Rivières, Trois-Rivières, QC, Canada.
Centre d'Excellence en Recherche sur les Maladies Orphelines - Fondation Courtois, Université du Québec à Trois-Rivières, Trois-Rivières, QC, Canada.
Front Pharmacol. 2020 Aug 28;11:578599. doi: 10.3389/fphar.2020.578599. eCollection 2020.
SARS-CoV-2 is a positive sense RNA coronavirus that constitutes a new threat for the global community and economy. While vaccines against SARS-CoV-2 are being developed, the mechanisms through which this virus takes control of an infected cell to replicate remains poorly understood. Upon infection, viruses completely rely on host cell molecular machinery to survive and replicate. To escape from the immune response and proliferate, viruses strategically modulate cellular metabolism and alter subcellular organelle architecture and functions. One way they do this is by modulating the structure and function of mitochondria, a critical cellular metabolic hub but also a key platform for the regulation of cellular immunity. This versatile nature of mitochondria defends host cells from viruses through several mechanisms including cellular apoptosis, ROS signaling, MAVS activation and mitochondrial DNA-dependent immune activation. These events are regulated by mitochondrial dynamics, a process by which mitochondria alter their structure (including their length and connectivity) in response to stress or other cues. It is therefore not surprising that viruses, including coronaviruses hijack these processes for their survival. In this review, we highlight how positive sense RNA viruses modulate mitochondrial dynamics and metabolism to evade mitochondrial mediated immune response in order to proliferate.
严重急性呼吸综合征冠状病毒2(SARS-CoV-2)是一种正链RNA冠状病毒,对全球社会和经济构成了新的威胁。虽然针对SARS-CoV-2的疫苗正在研发中,但这种病毒控制受感染细胞进行复制的机制仍知之甚少。感染后,病毒完全依赖宿主细胞的分子机制来生存和复制。为了逃避免疫反应并增殖,病毒会战略性地调节细胞代谢,改变亚细胞器的结构和功能。它们实现这一目的的一种方式是调节线粒体的结构和功能,线粒体是细胞代谢的关键枢纽,也是调节细胞免疫的关键平台。线粒体的这种多功能特性通过多种机制保护宿主细胞免受病毒侵害,包括细胞凋亡、活性氧信号传导、线粒体抗病毒信号蛋白(MAVS)激活和线粒体DNA依赖性免疫激活。这些事件受线粒体动力学调节,线粒体动力学是线粒体响应压力或其他信号改变其结构(包括长度和连接性)的过程。因此,包括冠状病毒在内的病毒劫持这些过程以实现生存也就不足为奇了。在这篇综述中,我们强调正链RNA病毒如何调节线粒体动力学和代谢,以逃避线粒体介导的免疫反应从而实现增殖。