About this Research Topic
Coronavirus disease 2019 (COVID-19) is associated with a pro-thrombotic state resulting in thrombotic microangiopathy and increased risk of venous thromboembolism and arterial thrombosis. Endothelial activation and immunothrombotic responses are contributing factors in the hypercoagulability of COVID-19.
Studies have found enhanced formation of Neutrophil Extracellular Traps (NETs), complement activation and contact activation. Platelets may both be activated by and contribute to the above mechanisms. A few small studies have demonstrated platelet hyper-reactivity and increased platelet-leukocyte interactions in COVID-19 patients but overall evidence on the role of platelets in COVID-19 is limited. Potential effects of anti-platelet treatments are also largely unknown.
Platelets have immunological functions via for instance Toll-like receptors (TLR’s) and may be directly activated by viruses in the circulation. Platelets interact both with the inflamed endothelium and immune cells and are involved in leukocyte recruitment to the vessel wall. Platelets have receptors for cytokines that are elevated in COVID-19, including TNF-α and IL-6, and also release inflammatory chemokines such as MCP-1, soluble CD40L, platelet factor 4 (PF4) and RANTES. Further platelets can stimulate NETosis and are activated by NETs.
We welcome original articles, reviews, hypotheses/theory and opinion papers clarifying the role of platelets in COVID-19 pathophysiology and micro-/macrothrombosis.
Topics may include (but are not limited to) the following areas:
1) Platelet activation mechanisms in COVID-19.
2) Importance of pre-morbid platelet hyper-reactivity on COVID-19 thrombosis, in particular for patients with established COVID-19 risk factors such as diabetes, hypertension, obesity and cardiovascular disease, which are associated with enhanced platelet reactivity.
3) Importance of individual variations in platelet phenotype response for COVID-19 hypercoagulability, e g propensity to form coated/pro-coagulant platelets,
4) Differences in interactions between platelets and SARS-CoV-2 compared to RNA viruses causing mainly hemorrhaghic symptoms (eg dengue virus, lassa virus).
5) The possible role of pulmonary megakaryocytes in COVID-19.
6) Influence of platelet inhibitors on COVID-19 disease severity and risk of thrombosis.
7) Potential differences between aspirin and P2Y12-inhibitors on COVID-19 platelet response and platelet-leukocyte interactions.
8) Effects of alternative platelet inhibitors, such as dipyridamole, cilostazol, PAR-1 receptor inhibitor and GPIIbIIIa inhibitors.
Studies have found enhanced formation of Neutrophil Extracellular Traps (NETs), complement activation and contact activation. Platelets may both be activated by and contribute to the above mechanisms. A few small studies have demonstrated platelet hyper-reactivity and increased platelet-leukocyte interactions in COVID-19 patients but overall evidence on the role of platelets in COVID-19 is limited. Potential effects of anti-platelet treatments are also largely unknown.
Platelets have immunological functions via for instance Toll-like receptors (TLR’s) and may be directly activated by viruses in the circulation. Platelets interact both with the inflamed endothelium and immune cells and are involved in leukocyte recruitment to the vessel wall. Platelets have receptors for cytokines that are elevated in COVID-19, including TNF-α and IL-6, and also release inflammatory chemokines such as MCP-1, soluble CD40L, platelet factor 4 (PF4) and RANTES. Further platelets can stimulate NETosis and are activated by NETs.
We welcome original articles, reviews, hypotheses/theory and opinion papers clarifying the role of platelets in COVID-19 pathophysiology and micro-/macrothrombosis.
Topics may include (but are not limited to) the following areas:
1) Platelet activation mechanisms in COVID-19.
2) Importance of pre-morbid platelet hyper-reactivity on COVID-19 thrombosis, in particular for patients with established COVID-19 risk factors such as diabetes, hypertension, obesity and cardiovascular disease, which are associated with enhanced platelet reactivity.
3) Importance of individual variations in platelet phenotype response for COVID-19 hypercoagulability, e g propensity to form coated/pro-coagulant platelets,
4) Differences in interactions between platelets and SARS-CoV-2 compared to RNA viruses causing mainly hemorrhaghic symptoms (eg dengue virus, lassa virus).
5) The possible role of pulmonary megakaryocytes in COVID-19.
6) Influence of platelet inhibitors on COVID-19 disease severity and risk of thrombosis.
7) Potential differences between aspirin and P2Y12-inhibitors on COVID-19 platelet response and platelet-leukocyte interactions.
8) Effects of alternative platelet inhibitors, such as dipyridamole, cilostazol, PAR-1 receptor inhibitor and GPIIbIIIa inhibitors.
Keywords: platelet function, covid-19, thrombotic microangiopathy, venous thromboembolism, arterial thrombosis, Platelet activation, platelet inhibitors, dipyridamole, cilostazol, PAR-1 receptor inhibitor, GPIIbIIIa inhibitors, platelet aggregation, antiplatelet treatment
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
