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 reports suggested that the pulmonary failure seen in COVID-19 may not be solely driven by acute ARDS, but also microvascular thrombotic events, likely driven by complement activation. However, it is not fully understood how the SARS-CoV-2 infection mechanisms mediate thrombotic events, and whether such mechanisms and responses are unique to SARS-CoV-2 infection, compared to other respiratory infections. We address these questions here, in the context of normal lung epithelia, in vitro and in vivo, using publicly available data. Our results indicate that plasmin is a crucial mediator which primes interactions between complement and platelet-activating systems in lung epithelia upon SARS-CoV-2 infection, with a potential for therapeutic intervention.

中文翻译：

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血浆纤溶酶通过补体和血小板激活系统介导SARS-CoV-2感染中的溶栓事件

最近出现的β-冠状病毒SARS-CoV-2导致了当前的大流行，命名为COVID-19。COVID-19表现为严重疾病，表现为全身性炎症反应综合征，急性呼吸窘迫综合征（ARDS），血栓形成事件和休克，并存病和年龄进一步加剧。最近的临床报告表明，在COVID-19中看到的肺衰竭可能不仅是由急性ARDS引起的，而且还可能是由补体激活引起的微血管血栓形成事件。但是，与其他呼吸道感染相比，SARS-CoV-2感染机制是如何介导血栓形成事件的，以及与SARS-CoV-2感染相比，这种机制和反应是否是唯一的尚不完全清楚。在正常的肺上皮细胞体外和体内，我们在这里解决这些问题，使用公开可用的数据。我们的结果表明，纤溶酶是一种重要的介质，在SARS-CoV-2感染后，它可以引发肺上皮中补体与血小板激活系统之间的相互作用，具有治疗干预的潜力。