Infection with SARS-CoV-2, the causative agent of COVID-19, causes mild to moderate disease in most patients but carries a risk of morbidity and mortality. Seriously affected individuals manifest disorders of hemostasis and a cytokine storm, but it is not understood how these manifestations of severe COVID-19 are linked. Here, we showed that the SARS-CoV-2 spike protein engaged the CD42b receptor to activate platelets via 2 distinct signaling pathways and promoted platelet-monocyte communication through the engagement of P selectin/PGSL-1 and CD40L/CD40, which led to proinflammatory cytokine production by monocytes. These results explain why hypercoagulation, monocyte activation, and a cytokine storm are correlated in patients severely affected by COVID-19 and suggest a potential target for therapeutic intervention.

中文翻译：

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血小板通过 SARS-CoV-2 刺突蛋白介导炎性单核细胞活化

感染 COVID-19 的病原体 SARS-CoV-2 会导致大多数患者出现轻度至中度疾病，但存在发病和死亡的风险。严重受影响的个体表现出止血障碍和细胞因子风暴，但尚不清楚严重 COVID-19 的这些表现是如何联系起来的。在这里，我们发现 SARS-CoV-2 刺突蛋白通过 2 条不同的信号通路与 CD42b 受体结合激活血小板，并通过 P 选择素/PGSL-1 和 CD40L/CD40 的结合促进血小板-单核细胞通讯，从而导致促炎。单核细胞产生细胞因子。这些结果解释了为什么高凝、单核细胞活化和细胞因子风暴在受 COVID-19 严重影响的患者中相关，并提出了治疗干预的潜在目标。