About this Research Topic

Background

Platelets are increasingly recognized for their role as mediators of immune response and inflammation. As major components of the hematological system, they form an important bridge between immunity and coagulation. In the context of viral infections, platelets may suppress viral dissemination but can also support viral persistence. When platelets become hyperactivated in response to an infection, patients can develop immuno-thrombosis and coagulopathy. These derangements of hemostasis are particularly relevant in the context of infection with the novel coronavirus, SARS-CoV-2, and the subsequent development of coronavirus disease, COVID-19, a disease in which thromboembolic events are an important cause of morbidity and mortality.
Many studies have demonstrated hyperactivation of platelets in persons infected with SARS-CoV-2, especially in those with severe disease. This in vivo hyperactivation can be associated with a subsequent hyporesponsiveness in vitro, in some assays and some reports.
The exact mechanism for interaction between SARS-CoV-2 and platelets is, however, poorly understood. The ACE2 receptor and cellular serine protease TMPRSS2 that appear to be the primary mechanism for SARS-CoV-2 entry into nasopharyngeal cells are not generally identified in platelets.
In addition, it is still poorly understood how platelet interactions with the endothelium mediate the development of thrombosis, especially in people with comorbidities that have been associated with poor outcomes, such as hypertension, cardiovascular disease and obesity. It appears that platelet hyperactivity and high levels of underlying inflammation play important roles, but there are many unanswered questions. In this regard, the exact role of platelet interactions with neutrophils and lymphocytes, as well as the production of complement-mediated neutrophil extracellular traps and eventual thrombocytopenia still needs to be elucidated. Increasing our understanding on immunoregulatory functions of platelets in viral infections will undoubtedly improve our knowledge of disease pathogenesis, clinical management, and therapeutic options.
In this Research Topic, we welcome the submission of Original Research, Review, Mini-Review, and Opinion articles that cover different aspects of the immunological role of platelet activation in the pathophysiology of COVID-19. We specifically encourage studies that cover, but are not limited to, to the following topics:
1. Immune interactions of SARS-CoV-2 with platelets, including the role of platelets in SARS-CoV-2 viral control or propagation2. The role of platelet immune activation in the development of COVID-19-related thromboembolic events 3. COVID-19-related coagulopathy-associated alterations in platelet immune function, including effects of SARS-CoV-2 on research and clinical laboratory assessments of platelet function4. Platelets as a diagnostic and prognostic marker of immune events and/or thromboinflammation in COVID-195. How does platelet immune functionality differ during SARS-CoV-2 infection when compared with other pulmonary infections and non-infectious acute lung inflammatory disorders (such as ARDS or TRALI)?6. Immune response involving platelets to various COVID-19 treatments, including corticosteroids, antivirals (such as remdesivir), convalescent plasma, and others.

Topic Editor Dr. Wool is on the clinical advisory board and receives honoraria from Diagnostica Stago. The other Topic Editors declare no competing interests with regards to the Research Topic subject

Keywords: platelet, innate immunity, COVID-19

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.

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