COVID-19 can result in severe disease characterized by significant immunopathology that is spurred by an exuberant, yet dysregulated, innate immune response with a poor adaptive response. A limited and delayed interferon I (IFN-I) and IFN-III response results in exacerbated proinflammatory cytokine production and in extensive cellular infiltrates in the respiratory tract, resulting in lung pathology. The development of effective therapeutics for patients with severe COVID-19 depends on our understanding of the pathological elements of this unbalanced innate immune response. Here, we review the mechanisms by which SARS-CoV-2 both activates and antagonizes the IFN and inflammatory response following infection, how a dysregulated cytokine and cellular response contributes to immune-mediated pathology in COVID-19, and therapeutic strategies that target elements of the innate response.

COVID-19 可导致严重的疾病，其特征是显着的免疫病理学，这是由旺盛但失调的先天免疫反应和较差的适应性反应引起的。有限且延迟的干扰素 I (IFN-I) 和 IFN-III 反应会导致促炎细胞因子的产生加剧以及呼吸道中广泛的细胞浸润，从而导致肺部病变。针对重症 COVID-19 患者的有效治疗方法的开发取决于我们对这种不平衡的先天免疫反应的病理因素的理解。在这里，我们回顾了 SARS-CoV-2 在感染后激活和拮抗 IFN 和炎症反应的机制，失调的细胞因子和细胞反应如何导致 COVID-19 中免疫介导的病理学，