Coronavirus disease 2019 (COVID-19), the current pandemic disease, is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Type I and III interferons (IFNs) are innate cytokines that are important in the first-line defense against viruses. Similar to many other viruses, SARS-CoV-2 has evolved mechanisms for evading the antiviral effects of type I and III IFNs at multiple levels, including the induction of IFN expression and cellular responses to IFNs. In this review, we describe the innate sensing mechanisms of SARS-CoV-2 and the mechanisms used by SARS-CoV-2 to evade type I and III IFN responses. We also discuss contradictory reports regarding impaired and robust type I IFN responses in patients with severe COVID-19. Finally, we discuss how delayed but exaggerated type I IFN responses can exacerbate inflammation and contribute to the severe progression of COVID-19.

冠状病毒病 2019 (COVID-19) 是当前的大流行病，由严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 感染引起。I 型和 III 型干扰素 (IFN) 是先天性细胞因子，在抵御病毒的一线防御中很重要。与许多其他病毒相似，SARS-CoV-2 已经进化出多种机制来逃避 I 型和 III 型 IFN 的抗病毒作用，包括诱导 IFN 表达和细胞对 IFN 的反应。在这篇综述中，我们描述了 SARS-CoV-2 的先天感知机制以及 SARS-CoV-2 用于逃避 I 型和 III 型 IFN 反应的机制。我们还讨论了关于严重 COVID-19 患者 I 型 IFN 反应受损和强健的相互矛盾的报告。最后，