Department of Bioactive Material Science, Korea Zoonosis Research Institute and Genetic Engineering Research Institute, Jeonbuk National University, Jeonju 54531, Korea.
Center for Convergent Research of Emerging Virus Infection, Korea Research Institute of Chemical Technology, Daejeon 34114, Korea.
Viruses. 2022 Mar 4;14(3):530. doi: 10.3390/v14030530.
In the past 20 years, coronaviruses (CoVs), including SARS-CoV-1, MERS-CoV, and SARS-CoV-2, have rapidly evolved and emerged in the human population. The innate immune system is the first line of defense against invading pathogens. Multiple host cellular receptors can trigger the innate immune system to eliminate invading pathogens. However, these CoVs have acquired strategies to evade innate immune responses by avoiding recognition by host sensors, leading to impaired interferon (IFN) production and antagonizing of the IFN signaling pathways. In contrast, the dysregulated induction of inflammasomes, leading to uncontrolled production of IL-1 family cytokines (IL-1β and IL-18) and pyroptosis, has been associated with COVID-19 pathogenesis. This review summarizes innate immune evasion strategies employed by SARS-CoV-1 and MERS-CoV in brief and SARS-CoV-2 in more detail. In addition, we outline potential mechanisms of inflammasome activation and evasion and their impact on disease prognosis.
在过去的 20 年中，冠状病毒（CoV），包括 SARS-CoV-1、MERS-CoV 和 SARS-CoV-2，在人类中迅速进化和出现。先天免疫系统是抵御入侵病原体的第一道防线。多种宿主细胞受体可以触发先天免疫系统来消除入侵的病原体。然而，这些 CoV 通过避免被宿主传感器识别而获得了逃避先天免疫反应的策略，导致干扰素（IFN）产生受损和 IFN 信号通路受到拮抗。相比之下，细胞焦亡相关的炎性小体的失调诱导，导致白细胞介素（IL）-1 家族细胞因子（IL-1β 和 IL-18）和细胞焦亡的不受控制产生，与 COVID-19 的发病机制有关。本综述简要总结了 SARS-CoV-1 和 MERS-CoV 采用的先天免疫逃避策略，并更详细地介绍了 SARS-CoV-2 的策略。此外，我们还概述了炎性小体激活和逃避的潜在机制及其对疾病预后的影响。
