Faculty of Applied Sciences and Biotechnology, Shoolini University of Biotechnology and Management Sciences, Bajhol, Himachal Pradesh 173229, India.
Department of Virology, Post Graduate Institute of Medical Education and Research, (PGIMER), Sec-12, Chandigarh 160012, India.
Med Hypotheses. 2021 Jan;146:110371. doi: 10.1016/j.mehy.2020.110371. Epub 2020 Nov 6.
The universal phenomenon of blood clotting is well known to be protective in external cellular/ tissue injury. However, the emergence of unusual thrombotic presentations in COVID-19 patients is the real concern. Interaction of the spike glycoprotein with ACE2 receptor present in the host cell surface mediates the entry of SARS-CoV-2 causing COVID-19 infection. New clinical findings of SARS-CoV-2 pathogenesis are coming out every day, and one such mystery is the formation of mysterious blood clots in the various tissues and organs of COVID-19 patients, which needs critical attention. To address this issue, we hypothesis that, high ACE2 expression in the endothelium of blood vessels facilitates the high-affinity binding of SARS-CoV-2 using spike protein, causing infection and internal injury inside the vascular wall of blood vessels. This viral associated injury may directly/indirectly initiate activation of coagulation and clotting cascades forming internal blood clots. However, the presence of these clots is undesirable as they are responsible for thrombosis and need to be treated with anti-thrombotic intervention.
众所周知,血液凝结的普遍现象在细胞/组织外部损伤中具有保护作用。然而,COVID-19 患者出现异常的血栓形成表现才是真正令人担忧的。刺突糖蛋白与宿主细胞表面存在的 ACE2 受体相互作用介导了 SARS-CoV-2 进入,导致 COVID-19 感染。SARS-CoV-2 发病机制的新临床发现每天都在出现,其中一个谜团是 COVID-19 患者的各种组织和器官中形成神秘的血栓,这需要引起重视。为了解决这个问题,我们假设血管内皮细胞中 ACE2 的高表达有助于 SARS-CoV-2 利用刺突蛋白进行高亲和力结合,从而导致血管血管壁内的感染和内部损伤。这种与病毒相关的损伤可能直接/间接启动凝血和血栓形成级联反应,形成内部血栓。然而,这些血栓的存在是不理想的,因为它们会导致血栓形成,需要进行抗血栓干预治疗。