De Michele et al.: "Evidence of SARS-CoV-2 spike protein on retrieved thrombi from COVID-19 patients"; indicates that SARS-CoV-2 Spike Protein may drive blood clots

"found SARS-CoV-2 Spike protein directly attached to platelets within the blood retrieved clots"

SOURCE:

https://jhoonline.biomedcentral.com/articles/10.1186/s13045-022-01329-w?utm_source=substack&utm_medium=email#:~:text=It%20has%20been%20observed%20that,or%20endothelial%20cells%20%5B1%5D.

‘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.’

This statement “we could detect SP, but not nucleocapsid protein, on platelets of COVID-19 patients’ thrombi” is critical. SP (spike protein) alone on platelets of COVID-19 patients’ thrombi suggests this is due to vaccine and not natural infection. If nucleocapsid protein is detected (with SP), then this suggests natural infection (natural immunity). This raises the distinct probability that the spike protein (certainly via the vaccine) is pathological and involved with the blood clotting sequelae.