COVID-19 induces a hyperactive phenotype in circulating platelets

Abstract

Background Coronavirus disease 2019 (COVID-19), caused by novel coronavirus SARS-CoV-2, has to date affected over 13.3 million globally. Although high rates of venous thromboembolism and evidence of COVID-19-induced endothelial dysfunction have been reported, the precise aetiology of the increased thrombotic risk associated with COVID-19 infection remains to be fully elucidated. Objectives Here, we assessed clinical platelet parameters and circulating platelet activity in patients with severe and non-severe COVID-19. Methods An assessment of clinical blood parameters in patients with severe COVID-19 disease (requiring intensive care), patients with non-severe disease (not requiring intensive care), general medical in-patients without COVID-19 and healthy donors was undertaken. Platelet function and activity were also assessed by secretion and specific marker analysis. Results We show that routine clinical blood parameters including increased MPV and decreased platelet:neutrophil ratio are associated with disease severity in COVID-19 upon hospitalisation and intensive care unit admission. Strikingly, agonist-induced ADP release was dramatically higher in COVID-19 patients compared with non-COVID-19 hospitalized patients and circulating levels of PF4, sP-selectin and TPO were also significantly elevated in COVID-19. Conclusion Distinct differences exist in routine full blood count and other clinical laboratory parameters between patients with severe and non-severe COVID-19. Moreover, we have determined that COVID-19 patients possess hyperactive circulating platelets. These data suggest that abnormal platelet reactivity may contribute to hypercoagulability in COVID-19. Further investigation of platelet function in COVID-19 may provide additional insights into the aetiology of thrombotic risk in this disease and may contribute to the optimisation of thrombosis prevention and treatment strategies.

Soluble P-selectin as a potential diagnostic and prognostic biomarker for COVID-19 disease: A case-control study

“…More recently, Comer et al found higher levels of sP-Selectin in patients with COVID-19 infection. Moreover, a higher sP-Selectin level was found in severe COVID-19 patients compared to the non-severe COVID group [ 35 ]. In another study, although Agrati et al found serum sP-Selectin level to be high in COVID-19 patients, there was no difference in sP-Selectin level in ICU and Non-ICU groups [ 19 ].…”

Mean Platelet Volume Predicts Severe COVID-19 Illness

“…A total number of 18 studies were finally included in our analysis, with 3,433 COVID-19 patients, 780 (22.7%) with severe illness (►Table 1). [6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] All except two were crosssectional studies, with the majority from China (7; 39%), and used heterogeneous combination of clinical endpoints for defining severity of COVID-19 (44% included respiratory failure and/or intensive care unit admission, 33% death, and 6% acute kidney failure or thrombosis; ►Table 1).…”

KLF2 is a therapeutic target for COVID-19 induced endothelial dysfunction

“…Emerging histopathological evidence from COVID-19 patients have underscored the pivotal role of endothelial cell dysfunction, thrombosis/coagulation, and systemic inflammation in COVID-19 caused by SARS-CoV-2 infection (3, 18). Consecutive inflammatory/immune cell recruitment and endothelial dysfunction could explain microcirculation failure and systemic endotheliitis observed in various vascular beds (15, 19).…”