Department of Surgery, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran.
Adv Exp Med Biol. 2021;1318:149-167. doi: 10.1007/978-3-030-63761-3_9.
Virus and host innate immune system interaction plays a significant role in forming the outcome of viral diseases. Host innate immunity initially recognizes the viral invasion and induces a rapid inflammatory response, and this recognition activates signaling cascades that trigger the release of antiviral mediators. This chapter aims to explore the mechanisms by which newly emerged coronavirus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) activates the host immune system. Since SARS-CoV-2 shares similarities with SARS-CoV that caused the epidemic of SARS in 2003, the pathogenesis of both viruses could be at least very similar. For this, this chapter provides a synthesis of literature concerning antiviral immunity in SARS-CoV and SARS-CoV-2. It includes the presentation of epitopes linked to SARS-CoV-2 as well as the ability of SARS-CoV-2 to cause proteolytic activation and interact with angiotensin-converting enzyme 2 (ACE2) via molecular mimicry. This chapter characterizes various mechanisms that this virus may engage in escaping the host immunity, ended by a discussion of humoral immune responses against SARS-CoV-2.
病毒和宿主固有免疫系统的相互作用在形成病毒疾病的结果方面起着重要作用。宿主固有免疫最初识别病毒入侵并诱导快速炎症反应，这种识别激活信号级联反应，触发抗病毒介质的释放。本章旨在探讨新型冠状病毒（称为严重急性呼吸综合征冠状病毒 2，SARS-CoV-2）激活宿主免疫系统的机制。由于 SARS-CoV-2 与 2003 年引起 SARS 流行的 SARS-CoV 具有相似性，因此两种病毒的发病机制至少非常相似。为此，本章综合了有关 SARS-CoV 和 SARS-CoV-2 抗病毒免疫的文献。它包括与 SARS-CoV-2 相关的表位的介绍，以及 SARS-CoV-2 通过分子模拟引起蛋白水解激活和与血管紧张素转换酶 2（ACE2）相互作用的能力。本章描述了该病毒可能逃避宿主免疫的各种机制，最后讨论了针对 SARS-CoV-2 的体液免疫反应。
