Cox Dermot
School of Pharmacy and Biomolecular Sciences, Royal College of Surgeons in Ireland, Dublin, Ireland.
Front Pharmacol. 2021 Jul 5;12:708665. doi: 10.3389/fphar.2021.708665. eCollection 2021.
It is clear that COVID-19 is more than a pneumonia and is associated with a coagulopathy and multi-organ failure. While the use of anti-coagulants does reduce the incidence of pulmonary emboli, it does not help with survival. This suggests that the coagulopathy is more likely to be platelet-driven rather than thrombin-driven. There is significant evidence to suggest that SARS-CoV-2 virions directly interact with platelets to trigger activation leading to thrombocytopenia and thrombosis. I propose a model of multiple interactions between SARS-CoV-2 and platelets that has many similarities to that with and Dengue virus. As platelet activation and thrombosis are major factors in poor prognosis, therapeutics that target the platelet-SARS-CoV-2 interaction have potential in treating COVID-19 and other virus infections.
显然，新冠病毒肺炎不仅仅是一种肺炎，还与凝血病和多器官功能衰竭有关。虽然使用抗凝剂确实能降低肺栓塞的发生率，但对生存率并无帮助。这表明凝血病更可能是由血小板驱动而非凝血酶驱动。有大量证据表明，新冠病毒颗粒直接与血小板相互作用，触发激活，导致血小板减少和血栓形成。我提出了一个新冠病毒与血小板之间多重相互作用的模型，该模型与寨卡病毒和登革热病毒的模型有许多相似之处。由于血小板激活和血栓形成是预后不良的主要因素，针对血小板与新冠病毒相互作用的疗法在治疗新冠病毒肺炎和其他病毒感染方面具有潜力。
