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Abstract：
SARS-CoV-2 was identified as the causative pathogen in an outbreak of viral pneumonia cases originating in Wuhan, China, with an ensuing rapid global spread that led it to be declared a pandemic by the WHO on March 11, 2020. Given the threat to public health posed by sequelae of SARS-CoV-2 infection, the literature surrounding patient presentation in severe and non-severe cases, transmission rates and routes, management strategies, and initial clinical trial results have become available at an unprecedented pace. In this review we collate current clinical and immunologic reports, comparing these to reports of previous coronaviruses to identify mechanisms driving progression to severe disease in some patients. In brief, we propose a model wherein dysregulated type I interferon signalling leads to aberrant recruitment and accumulation of innate immune lineages in the lung, impairing establishment of productive adaptive responses, and permitting a pathologic pro-inflammatory state. Finally, we extend these findings to suggest possible treatment options that may merit investigation in randomized clinical trials.
摘要：
SARS-CoV-2在武汉爆发的病毒性肺炎病例中被确定为病原体，中国,随之而来的全球迅速传播，导致它在2020年3月11日被世卫组织宣布为大流行。鉴于SARS-CoV-2感染后遗症对公众健康的威胁，围绕重症和非重症病例患者表现的文献，传输速率和路线，管理策略，和初步的临床试验结果已经成为前所未有的速度。在这篇综述中，我们整理了当前的临床和免疫学报告，将这些与以前的冠状病毒报告进行比较，以确定某些患者导致严重疾病进展的机制。简而言之,我们提出了一个模型，其中失调的I型干扰素信号导致肺部先天免疫谱系的异常募集和积累，损害生产性适应性反应的建立，并允许病理性促炎状态。最后,我们扩展了这些发现,提出了可能值得在随机临床试验中研究的治疗方案.
