Pathogens usurp host pathways to generate a permissive environment for their propagation. The current spread of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection presents the urgent need to understand the complex pathogen–host interplay for effective control of the virus. SARS-CoV-2 reorganizes the host cytoskeleton for efficient cell entry and controls host transcriptional processes to support viral protein translation. The virus also dysregulates innate cellular defenses using various structural and nonstructural proteins. This results in substantial but delayed hyperinflammation alongside a weakened interferon (IFN) response. We provide an overview of SARS-CoV-2 and its uniquely aggressive life cycle and discuss the interactions of various viral proteins with host signaling pathways. We also address the functional changes in SARS-CoV-2 proteins, relative to SARS-CoV. Our comprehensive assessment of host signaling in SARS-CoV-2 pathogenesis provides some complex yet important strategic clues for the development of novel therapeutics against this rapidly emerging worldwide crisis.

病原体篡夺宿主途径，为其传播创造一个宽松的环境。当前严重急性呼吸系统综合症冠状病毒 2 (SARS-CoV-2) 感染的传播表明，迫切需要了解复杂的病原体-宿主相互作用，以有效控制该病毒。SARS-CoV-2 重组宿主细胞骨架以有效进入细胞并控制宿主转录过程以支持病毒蛋白翻译。该病毒还使用各种结构和非结构蛋白来调节先天细胞防御。这会导致严重但延迟的过度炎症以及减弱的干扰素 (IFN) 反应。我们概述了 SARS-CoV-2 及其独特的侵袭性生命周期，并讨论了各种病毒蛋白与宿主信号通路的相互作用。我们还解决了 SARS-CoV-2 蛋白相对于 SARS-CoV 的功能变化。我们对 SARS-CoV-2 发病机制中宿主信号传导的综合评估为针对这一迅速出现的全球危机开发新疗法提供了一些复杂但重要的战略线索。