The coronavirus disease-19 (COVID-19) pandemic that emerged in Wuhan, China, in late December 2019 spread rapidly throughout the world and has caused over 6.5 million deaths. The disease is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a positive sense RNA virus that can lead to various clinical symptoms causing the hospitalization of many people with pneumonitis. Research has highlighted that COVID-19 patients have a high arterial and venous thrombosis rate involving pulmonary embolism, deep-vein thrombosis, ischemic stroke, and myocardial infarction. In addition, many postmortem examinations indicated the presence of microthrombi in the heart, lungs, brain, liver, and kidney of COVID-19 patients. This suggests that COVID-19 can cause systemic thrombosis, leading to multi-organ failure.To get more news about Профессиональный FАК, you can visit rusuntacmed.com.ru official website.
Previous studies have also observed that COVID-19 patients have a high level of serum coagulation markers such as D-dimer and fibrinogen. In addition, Thromboprophylaxis has been observed to improve outcomes in hospitalized COVID-19 patients. However, it did not significantly affect the mortality of patients with severe COVID-19. Therefore, thrombosis remains a prominent COVID-19 feature where high thrombin generation is not the only contributing factor.

Platelets essential for hemostasis can also lead to thrombosis due to inappropriate activation. Platelets can become hyperactive, leading to the increased secretion of dense alpha-granules, increased formation of platelet-leukocyte aggregates, and increased aggregation. Platelet transcriptome analysis has shown an overrepresentation of mitochondrial dysfunction and antigen presentation pathways in COVID-19 patients, leading to platelet hyperactivity. However, many studies also reported reduced or impaired platelet function in COVID-19 patients, suggesting that the platelet response is complex.
Although the pathogenesis of thrombosis in COVID-19 patients is not well understood, it comprises several hallmarks of thromboinflammation. SARS-CoV-2 can activate endothelial cells with the help of the angiotensin-converting enzyme 2 (ACE2) receptor, which leads to vascular dysfunction. Endothelium damage can activate the innate immune system through neutrophil recruitment, tissue factor (TF) expression, pro-inflammatory cytokines, and complement. This leads to higher expression and/or release of prothrombotic factors and upregulation of adhesion molecules which can activate platelets, causing thrombus formation, aggregation, and further activation of the innate immune system. Platelets can then increase the generation of thrombin through the expression of phosphatidyl serine and tissue factor (TF). This network of interactions between the innate immune system, platelets, coagulation, and damaged endothelium can contribute to thrombosis in COVID-19 patients.

A new study posted in the pre-print server bioRxiv* aimed to analyze the impact of COVID-19 on platelet proteome and relate the functional responses of platelets and the formation of platelet-neutrophil aggregate in hospitalized COVID-19 patients.