PMC:7386875 / 26235-28861 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7386875","sourcedb":"PMC","sourceid":"7386875","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7386875","text":"To date, there is a relative paucity of data regarding how SARS-CoV-2 may influence platelet function and potentially contribute to the prothrombotic phenotype observed in patients with COVID-19. However, there is now a large body of evidence demonstrating that viruses can directly interact with platelets thus potentially modulating their thrombotic and inflammatory function.75,76 Indeed, platelets are endowed with a large repertoire of adhesion receptors and immune receptors such as TLRs, FcγRIIa, and CXC/CCL receptors in addition to possessing the ability to engulf virions. Influenza, like SARS-CoV-2, is a single-stranded RNA virus which has been demonstrated to activate platelets via TLR-7 and the FcγRIIa receptor. The activation of platelet TLR-7 by viral RNA can evoke a range of functional responses which support thrombus formation, including platelet degranulation, the formation of platelet-leukocyte aggregates and platelet C3 release which in turn stimulates NETosis.75–78 In addition, previous work focusing on platelet activation by viruses has demonstrated that HSV-1 (herpes simplex virus 1) can induce thrombi via FcγRIIa on platelets and that the influenza strain H1N1 can activate platelets, both in a FcγRIIa- and thrombin-dependent fashion, thus leading to platelet GPIIb/IIIa activation, arachidonic acid metabolism, and platelet microvesicle release.79,80 Corresponding mouse studies have emphasized an important role of platelets in H1N1 infection since mice infected with sublethal doses of H1N1 demonstrated large numbers of activated platelets in their lung tissue in addition to platelet-leukocyte aggregates and microvascular thrombosis.81 Interestingly, inhibition of the major platelet adhesion receptor, GPIIb/IIIa, resulted in a protection from fatal influenza and a reduction in lung inflammation and microvascular thrombosis.81 Moreover, recent studies have demonstrated that platelets from patients with influenza contain virus particles, while human platelets appear to have the ability to internalize the influenza virus.77 Thus, a key outstanding area of research regarding the effects of SARS-CoV-2 and thrombosis pertains to how this virus interacts with platelets to mediate platelet number and function. In this regard, understanding if SARS-CoV-2 can be internalized and activate platelet TLR-7 and whether the ACE-2 receptor is expressed on platelets remain core unanswered questions. This is likely to be critical to understanding the link between COVID-19 and the prothrombotic phenotype given the key role of platelets in co-ordinating the thromboinflammatory 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