The SARS‐CoV‐2 makes its way into the cell via the ACE2 receptor and the proteolytic action of TMPRSS2. In response to the SARS‐CoV‐2 infection, the innate immune response is the first line of defense, triggering multiple signaling pathways to produce interferons, pro‐inflammatory cytokines and chemokines, and initiating the adaptive immune response against the virus. Unsurprisingly, the virus has developed strategies to evade detection, which can result in delayed, excessive activation of the innate immune system. The response elicited by the host depends on multiple factors, including health status, age, and sex. An overactive innate immune response can lead to a cytokine storm, inflammation, and vascular disruption, leading to the vast array of symptoms exhibited by COVID‐19 patients. What is known about the expression and epigenetic regulation of the ACE2 gene and the various players in the host response are explored in this review.

中文翻译：

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SARS-CoV ‐2 与人类宿主的多方面相互作用。第二部分：先天免疫反应、免疫病理学和表观遗传学

SARS-CoV-2 通过 ACE2 受体和 TMPRSS2 的蛋白水解作用进入细胞。针对SARS-CoV-2感染，先天免疫反应是第一道防线，触发多种信号通路产生干扰素、促炎细胞因子和趋化因子，并启动针对病毒的适应性免疫反应。不出所料，该病毒已经开发出逃避检测的策略，这可能导致先天免疫系统的延迟过度激活。宿主引起的反应取决于多种因素，包括健康状况、年龄和性别。过度活跃的先天免疫反应会导致细胞因子风暴、炎症和血管破坏，从而导致 COVID-19 患者表现出的大量症状。