Procoagulant and fibrinolytic activity in COVID-19 infections as markers of disease progression & severity

COVID-19 is a disease that results from infection with a new coronavirus that emerged in late 2019 and has resulted in a worldwide pandemic. Up to a third of patients hospitalised for COVID-19 develop a severe form of lung disease that can be fatal. From similar diseases, including the common flu and pneumonia, we know that part of the problem is that the air space in the lung is consumed by deposits of scaffold protein, called fibrin, that form in the lining of the deep lung. These fibrin deposits restrict the amount of oxygen being absorbed by the lung and patients with severe disease require oxygen support, and in acute cases mechanical ventilation. We are interested in two key questions. Firstly, the mechanisms underlying how this excessive fibrin forms in the lungs of COVID-19 patients and secondly whether we can predict this from measuring fibrin forming (coagulation) and fibrin degradation (fibrinolysis) activity in the blood of these patients. Understanding why there is impaired fibrin turnover in the lungs of these critically ill COVID-19 patients and defining key molecules involved, will inform us on the most appropriate therapeutic treatments