Human coronavirus (HCoV) infection causes respiratory diseases with mild to severe outcomes. In the last 15 years, we have witnessed the emergence of two zoonotic, highly pathogenic HCoVs: severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV). Replication of HCoV is regulated by a diversity of host factors and induces drastic alterations in cellular structure and physiology. Activation of critical signaling pathways during HCoV infection modulates the induction of antiviral immune response and contributes to the pathogenesis of HCoV. Recent studies have begun to reveal some fundamental aspects of the intricate HCoV-host interaction in mechanistic detail. In this review, we summarize the current knowledge of host factors co-opted and signaling pathways activated during HCoV infection, with an emphasis on HCoV-infection-induced stress response, autophagy, apoptosis, and innate immunity. The cross talk among these pathways, as well as the modulatory strategies utilized by HCoV, is also discussed.

中文翻译：

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人类冠状病毒：宿主-病原体相互作用。

人冠状病毒（HCoV）感染可导致轻度至严重结局的呼吸道疾病。在过去的15年中，我们目睹了两种人畜共患的高致病性HCoV的出现：严重急性呼吸综合征冠状病毒（SARS-CoV）和中东呼吸综合征冠状病毒（MERS-CoV）。HCoV的复制受到多种宿主因素的调控，并诱导细胞结构和生理发生剧烈变化。HCoV感染过程中关键信号通路的激活可调节抗病毒免疫反应的诱导，并有助于HCoV的发病。最近的研究已经开始从机械细节上揭示复杂的HCoV-宿主相互作用的一些基本方面。在这篇综述中，我们总结了HCoV感染期间选择的宿主因子和激活的信号通路的最新知识，重点研究了HCoV感染引起的应激反应，自噬，细胞凋亡和先天免疫。还讨论了这些途径之间的串扰以及HCoV使用的调节策略。