Blood: Platelet activation and platelet-mononucleosis in patients with severe COVID-19 form trigger tissue factor expression.

The type 2 coronavirus (SARS-Cov-2) is a sudden pathogen of 2019 coronavirus disease (COVID-19).
since the emergence of the new coronavirus, it has rapidly reached pandemic levels, with significant increases in morbidity and mortality around the world.
reported that the high coagulation status is the main pathological event of COVID-19, and the complications of thromboembolism are classified as one of the life-threatening complications.
platelets are the main effect cells of hemostatic and pathological thrombosis.
but the role of platelets in COVID-19 pathogenesis remains unclear.
this report indicates that platelet activation and platelet-mononucleosis formation were observed in patients with severe COVID-19, but this phenomenon was not observed in patients with mild COVID-19 syndrome.
in addition, exposure to plasma in patients with severe COVID-19 increases the activation of controlled platelets.
platelet-mononucleosis is closely related to TF expression of mononucleocytes in the COVID-19 patient queue of the income ICU.
platelet activation and mononucleocellular TF expression are associated with markers of clotting dysfunction such as fibrinogen and D-dipolymers, and are elevated in patients who require invasive mechanical ventilation or who die in hospital.
finally, platelets in patients with COVID19 severe illness were able to induce TF expression in mononucleic cells in healthy volunteers, a phenomenon inhibited by platelet P-selectors and the agglomelateinhibitor axiosin alpha IIb/beta3.
in general, the study data highlighted a new pathogenic mechanism involving platelet activation and platelet-dependent mononucleosis, which is associated with the severity and mortality of COVID-19.
.