A group from Department of General and Laboratory Medicine, Mie Prefectural General Medical Center, Yokkaichi 510-0885, Japan, etc. has reported importance of the spike protein-induced direct platelet activation as a basis of COVID-19 pathogenesis.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8877880/
Several mechanisms underlying the worsening of the condition of COVID-19 patients have been proposed, for instance, cytokine storm, primary pulmonary thrombosis, vascular endothelial injuries, and platelet activation. One of the clinical features of COVID-19 is the high prevalence of arterial thrombosis such as stroke and ischemic heart disease. Therefore, it was assumed that the activation in platelets would be involved in the pathogenesis. On the other hand, soluble C-type lectin-like receptor 2 (sCLEC-2) has been discovered as a new biomarker of platelet activation.
In this study, the levels of plasma biomarkers, such as sCLEC-2 and D-dimer, in 46 patients with COVID-19 were measured and compared to those in 127 patients with other infections to determine the mechanism underlying the worsening of COVID-19 infection.
Plasma sCLEC-2 levels were significantly higher in patients with COVID-19 infection than in those with bacterial infections. On the other hand, plasma D-dimer levels were significantly higher in patients with bacterial infections than COVID-19 infection. These findings suggest that COVID-19 infection tends to facilitate platelet activation, while bacterial infections tend to facilitate fibrin generation.
Possible pathogenesis of worsening COVID-19:
SARS-CoV-2 spike protein activates platelets directly via apoptosis of lymphocytes and induces thrombosis.