Severe acute respiratory syndrome coronavirus 2 (SARS-CoV 2) was identified as a new coronavirus causing pneumonia and acute respiratory distress syndrome. It has become a pandemic, spreading particularly quickly across Europe and the US. Most deaths are related to severe acute respiratory distress syndrome, but other organ failures, such as acute kidney failure and acute cardiac injury, seem also related to the disease.1 Inflammatory response is highly increased in coronavirus disease 2019 (COVID-19) infection, and inflammation is known to favor thrombosis. High dimerized plasmin fragment D (D-dimer) levels and procoagulant changes in coagulation pathways were reported among patients with severe COVID-19.2,3 An elevated rate of venous and arterial thrombotic events associated with COVID-19 infection has also been reported.4,5 This case series reports a systematic assessment of deep vein thrombosis among patients in an intensive care unit (ICU) in France with severe COVID-19.
The spike (S) protein of SARS coronavirus (SARS-CoV) has been known to recognize and bind to host receptors, whose conformational changes then facilitate fusion between the viral envelope and host cell membrane, leading to viral entry into target cells. However, other functions of SARS-CoV S protein such as proteolytic cleavage and its implications to viral infection are incompletely understood. In this study, we demonstrated that the infection of SARS-CoV and a pseudovirus bearing the S protein of SARS-CoV was inhibited by a protease inhibitor Ben-HCl. Also, the protease Factor Xa, a target of Ben-HCl abundantly expressed in infected cells, was able to cleave the recombinant and pseudoviral S protein into S1 and S2 subunits, and the cleavage was inhibited by Ben-HCl. Furthermore, this cleavage correlated with the infectivity of the pseudovirus. Taken together, our study suggests a plausible mechanism by which SARS-CoV cleaves its S protein to facilitate viral infection.
Increased VTE reported in patients with coronavirus disease 2019 (COVID-19)1,2 leads some to recommend routine use of therapeutic anticoagulation.3 However, the incidence of VTE in patients with COVID-19 ranges widely, depending on a number of variables. We hypothesized that ICU patients experience increased symptomatic VTE compared with ward patients, despite standard prophylactic anticoagulation.
Increased VTE reported in patients with coronavirus disease 2019 (COVID-19)1,2 leads some to recommend routine use of therapeutic anticoagulation.3 However, the incidence of VTE in patients with COVID-19 ranges widely, depending on a number of variables. We hypothesized that ICU patients experience increased symptomatic VTE compared with ward patients, despite standard prophylactic anticoagulation.