The innate immune system is a powerful barrier against invading pathogens. Interferons (IFNs) are a major part of the cytokine-mediated anti-viral innate immune response. After recognition of a pathogen by immune sensors, signaling cascades are activated that culminate in the release of IFNs. These activate cells in an autocrine or paracrine fashion eventually setting cells in an anti-viral state via upregulation of hundreds of interferon-stimulated genes (ISGs). To evade the anti-viral effect of the IFN system, successful viruses like the pandemic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) evolved strategies to counteract both IFN induction and signaling. In fact, more than half of the about 30 proteins encoded by SARS-CoV-2 target the IFN system at multiple levels to escape IFN-mediated restriction. Here, we review recent insights into the molecular mechanisms used by SARS-CoV-2 proteins to suppress IFN production and the establishment of an anti-viral state.

先天免疫系统是抵御入侵病原体的强大屏障。干扰素 (IFN) 是细胞因子介导的抗病毒先天免疫反应的主要部分。在免疫传感器识别病原体后，信号级联被激活，最终导致 IFN 的释放。这些以自分泌或旁分泌方式激活细胞，最终通过上调数百个干扰素刺激基因 (ISG) 使细胞处于抗病毒状态。为了逃避 IFN 系统的抗病毒作用，大流行性严重急性呼吸系统综合症冠状病毒 2 (SARS-CoV-2) 等成功的病毒进化出抵消 IFN 诱导和信号传导的策略。事实上，SARS-CoV-2 编码的约 30 种蛋白质中有一半以上在多个水平上靶向 IFN 系统，以逃避 IFN 介导的限制。这里，