Emergency Department, Stroke Unit, Sapienza University of Rome, Viale del Policlinico, 155, 00161, Rome, Italy.
Department of Radiology, Oncology and Pathological Science, Sapienza University of Rome, Rome, Italy.
J Hematol Oncol. 2022 Aug 16;15(1):108. doi: 10.1186/s13045-022-01329-w.
The pathophysiology of COVID-19-associated coagulopathy is complex and not fully understood. SARS-CoV-2 spike protein (SP) may activate platelets and interact with fibrin(ogen). We aimed to investigate whether isolated SP can be present in clots retrieved in COVID-19 patients with acute ischemic stroke (by mechanical thrombectomy) and myocardial infarction. In this pilot study, we could detect SP, but not nucleocapsid protein, on platelets of COVID-19 patients' thrombi. In addition, in all three COVID-19 thrombi analyzed for molecular biology, no SARS-CoV-2 RNA could be detected by real-time polymerase chain reaction. These data could support the hypothesis that free SP, besides the whole virus, may be the trigger of platelet activation and clot formation in COVID-19.
COVID-19 相关凝血病的病理生理学较为复杂,尚未完全阐明。SARS-CoV-2 刺突蛋白(SP)可能会激活血小板并与纤维蛋白(原)相互作用。我们旨在研究在通过机械血栓切除术治疗的 COVID-19 急性缺血性脑卒中(acute ischemic stroke,AIS)和心肌梗死(myocardial infarction,MI)患者的血栓中是否存在分离的 SP。在这项初步研究中,我们可以在 COVID-19 患者的血栓中的血小板上检测到 SP,但未检测到核衣壳蛋白。此外,在对三个 COVID-19 血栓进行的分子生物学分析中,均未通过实时聚合酶链反应检测到 SARS-CoV-2 RNA。这些数据可能支持以下假说,即游离 SP 可能除了完整病毒之外,还是 COVID-19 中血小板激活和血栓形成的触发因素。