Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The ability of our cells to secrete type I interferons (IFN-Is) is essential for the control of virus replication and for effective antiviral immune responses; for this reason, viruses have evolved the means to antagonize IFN-I. Inhibition of IFN-I production is pronounced in SARS-CoV-2 infection, which can impair the adaptive immune response and exacerbate inflammatory disease at late stages of infection. However, therapeutic boosting of IFN-I offers a narrow time window for efficacy and safety. Here, we discuss how limits placed on IFN-I by SARS-CoV-2 shape the immune response and whether this might be countered with therapeutic approaches and vaccine design.

2019 年冠状病毒病 (COVID-19) 是由严重急性呼吸系统综合症冠状病毒 2 (SARS-CoV-2) 引起的传染病。我们的细胞分泌 I 型干扰素 (IFN-Is) 的能力对于控制病毒复制和有效的抗病毒免疫反应至关重要；出于这个原因，病毒已经进化出对抗 IFN-I 的方法。IFN-I 产生的抑制在 SARS-CoV-2 感染中很明显，这会损害适应性免疫反应并在感染后期加剧炎症性疾病。然而，IFN-I 的治疗加强为疗效和安全性提供了一个狭窄的时间窗口。在这里，我们讨论了 SARS-CoV-2 对 IFN-I 的限制如何影响免疫反应，以及这是否可以通过治疗方法和疫苗设计来抵消。