PMC:7386875 / 47321-50606 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":"Anticoagulation\nThe strikingly increased prevalence of thrombotic complications has led to many hospitals instituting the routine administration of strict VTE prophylaxis with either low molecular weight heparin or unfractionated heparin and also resulting in several groups using intermediate or full-dose anticoagulation to prevent these thromboembolic phenomena.137,138 Preliminary reports have suggested that low molecular weight heparin treatment reduces mortality in COVID-19 patients with an elevated D-dimer or elevated sepsis-induced coagulopathy score.139 The heparins are widely used anticoagulants which inhibit coagulation by the antithrombin mediated inhibition of FXa or thrombin. However, aside from their effects on anticoagulation, the heparins appear to have pleiotropic effects that may provide unique advantages in the context of viral infection, including anti-inflammatory effects by way of their ability to bind to danger-associated molecular patterns, such as HMGB-1, and proinflammatory cytokines.140,141 Unfractionated heparin has a similar structure as heparan sulfate, the sulfated polysaccharide present on cell surfaces and extracellular matrix, with repeating disaccharide units. In contrast, low molecular weight heparin is a modified heparin with shorter polysaccharide chains. Intriguingly, heparan sulfate has previously implicated as a docking site for a number of viruses, thus facilitating cellular attachment of the virus and subsequent viral infection.142,143 Indeed, heparin, acting as a decoy receptor for naturally expressed heparan sulfate, has been shown to inhibit the binding of the SARS coronavirus to cells in vitro.144 While ACE-2 is the major receptor that mediates viral entry into cells, heparan sulfate has previously been demonstrated to play an important role in facilitating coronavirus entry into cells by functioning as an adhesion receptor for the virus on the cell surface thereby allowing the increased density of viral particles on the cell surface which then facilitates ACE-2-mediated cell entry.145 Recent studies have directly investigated the link between heparin and SARS-CoV-2 and suggest that heparin can directly bind with the spike protein of the SARS-CoV-2 virus and, therefore, may have antiviral properties.146\nAnother interesting aspect of how the SARS-CoV-2 virus may be influenced by the use of heparin as anticoagulant is the previous observation that FXa can cleave the spike protein of SARS-CoV to render it more efficient in invading cells.147 However, to date, this aspect remains to be investigated with SARS-CoV-2. These data have led some groups to propose specifically engineered heparins for the treatment of COVID-19, while clinical trials are underway to investigate the effects of low dose, and full-dose, anticoagulation with heparin on clinical outcomes for patients with COVID-19 (URL: https://www.clinicaltrials.gov. Unique identifiers: NCT04344756 and NCT04345848).142 It is important to note that given the potential for heparin therapeutics to cause heparin-induced thrombocytopenia, but reassuringly, despite both thrombocytopenia and thrombosis being common complications of COVID-19, the development of heparin-induced thrombocytopenia appears limited to individual case 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