PMC:7386875 / 25567-31727 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":"COVID-19 and Platelets—Sentinels of Viral Infection and Modulators of Adaptive Immunity\nThe most well-studied effect of SARS-CoV-2 on platelets pertains to its effect on platelet number. Thrombocytopenia has been reported as a common finding in severe COVID-19 with a recent meta-analysis demonstrating that thrombocytopenia was associated with a 5-fold increased risk of severe disease.14,16,73,74 The degree of thrombocytopenia in severe COVID-19 is usually mild and does not appear to be a common feature in nonsevere COVID-19.73 Whether thrombocytopenia is a direct effect of SARS-CoV-2 or multifactorial in the setting of severe illness remains to be elucidated.\nTo 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 response.\nA prominent clinical feature of severe COVID-19 is the occurrence of respiratory decompensation typically 1 week after initial symptom onset.82 This clinical trajectory appears to correlate with the time course of the adaptive immune response to SARS-CoV-2, with T- and B-cell responses to SARS-CoV-2 being detected ≈1 week after symptom onset.46 Given it is postulated that this respiratory decompensation is driven by pulmonary microvascular thrombosis, understanding the intersection between thrombosis and the adaptive immune response to SARS-CoV-2 is of significant interest. These interactions are likely important since platelets have previously been demonstrated to be key modulators of adaptive immunity in the context of a range of inflammatory disorders. Platelets play an important role in regulating T-cell trafficking by facilitating the recruitment of T lymphocytes to sites of vascular injury or infection.83 Moreover, platelets enhance T-cell functional responses via multiple mechanisms. For example, platelets express major histocompatibility complex class 1 molecules and can, therefore, directly activate T cells in an major histocompatibility complex class 1 dependent manner,84 while platelet-derived PF-4 and serotonin can regulate Th17 expansion85 and naïve T-cell activation and proliferation,86 respectively. The importance of platelets in mediating T-cell recruitment and trafficking is underscored by data demonstrating that platelets play a fundamental role in the accumulation of cytotoxic T cells, and virus-induced organ damage, in a murine model of acute viral hepatitis.87 Akin to the bidirectional relationship between platelets and other leukocyte subsets, the activation of T cells amplifies platelet aggregation with more recent data highlighting an important role for T cells recruited to sites of venous thrombosis in orchestrating the inflammatory response and subsequent thrombus resolution.88,89\nIn addition to mediating T-cell functions, platelets can increase B-cell immunoglobulin (Ig)G1, IgG2, and IgG3 production.90 This is potentially significant in the setting of COVID-19 since the development of antiphospholipid antibodies, such as anti-β2 glycoprotein IgG antibodies, have been described in association with thrombosis in patients with COVID-19.91 In addition, a cohort study from France describes a large percentage of patients with severe COVID-19 demonstrate a detectable lupus anticoagulant.27 However, whether the presence of antiphospholipid antibodies in COVID-19 plays a role in COVID-19-associated thrombosis or represents merely an association remains to be established. Nevertheless, delineating how platelets modulate the adaptive immune response to SARS-CoV-2 and the role adaptive immunity plays in mediating thrombosis and organ injury will be crucial in uncovering novel therapeutic 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