Evidence of SARS-CoV-2 spike protein on retrieved thrombi from COVID-19 patients, 2022, De Michele et al

Abstract

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.

Open access, https://jhoonline.biomedcentral.com/articles/10.1186/s13045-022-01329-w

 

Small study, looking at four consecutive patients undergoing clot retrieval. Ancestral strain, between April and Nov 2020; acute patients, with PCR-positivity. Three with large vessel occlusion acute ischaemic stroke, one with acute myocardial infarction. Controls were PCR negative strokes (which does not exclude them having then or prior COVID).

They found spike protein in the thrombi, but no nucleocapsid protein or viral RNA. Spike positivity was much more in the the single MI patient. The spike protein seemed to be co-located with platelets.

Referencing evidence of free spike protein in plasma, and noting their study size limitations, they hypothesise that SP may be activating platelets and endothelial cells, leading to thrombus formation: possibly with a mechanism of abnormally glycosylated immune complexes (referencing this paper).