Objective: Recently emerged beta-coronavirus SARS-CoV-2, has resulted in the current pandemic designated COVID-19. COVID-19 manifests as severe illness exhibiting systemic inflammatory response syndrome, acute respiratory distress syndrome (ARDS), thrombotic events, and shock, exacerbated further by co-morbidities and age. Recent clinical evidence suggests that the development of ARDS and subsequent pulmonary failure result from a complex interplay between cell types (endothelial, epithelial and immune) within the lung promoting inflammatory infiltration and a pro-coagulative state. How the complex molecular events mediated by SARS-CoV-2 in infected lung epithelial cells lead to thrombosis and pulmonary failure, is yet to be fully understood. Methods: We address these questions here, using publicly available transcriptomic data in the context of lung epithelia affected by SARS-CoV-2 and other respiratory infections, in vitro. We then extend our results to the understanding of in vivo lung, using a publicly available COVID-19 lung transcriptomic study. Results and Conclusions: Our analysis indicates that there exists a complex interplay between the fibrinolytic system particularly plasmin, and the complement and platelet-activating systems upon SARS-CoV-2 infection, with a potential for therapeutic intervention.

中文翻译：

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纤溶酶级联通过补体和血小板激活系统介导 SARS-CoV-2 感染中的血栓事件

客观的：最近出现的 β 冠状病毒 SARS-CoV-2 导致了当前的大流行，称为 COVID-19。COVID-19 表现为严重疾病，表现为全身炎症反应综合征、急性呼吸窘迫综合征 (ARDS)、血栓形成事件和休克，并因合并症和年龄而进一步恶化。最近的临床证据表明，ARDS 的发展和随后的肺衰竭是由肺内细胞类型（内皮细胞、上皮细胞和免疫细胞）之间的复杂相互作用导致的，这些细胞类型促进了炎症浸润和促凝状态。SARS-CoV-2 在受感染的肺上皮细胞中介导的复杂分子事件如何导致血栓形成和肺功能衰竭，目前尚待完全了解。方法：我们在这里解决了这些问题，在体外使用受 SARS-CoV-2 和其他呼吸道感染影响的肺上皮细胞的公开可用的转录组数据。然后，我们使用公开的 COVID-19 肺转录组学研究将我们的结果扩展到对体内肺的理解。结果和结论：我们的分析表明，纤溶系统（尤其是纤溶酶）与 SARS-CoV-2 感染后的补体和血小板激活系统之间存在复杂的相互作用，具有治疗干预的潜力。