Conclusion
COVID-19 is a devastating disease that has affected the UK and our global community in unprecedented ways. The pathophysiology is complex with multiple systems likely contributing to the pro-thrombotic state including inflammation, platelet and neutrophil activation, endothelial cell dysfunction, NETs and complement factors. However the mechanism(s) that drives COVID-19 associated thromboinflammation has not yet been fully elucidated and there is an urgent unmet clinical need to fully understand and characterise this disease. These discoveries will unearth ways to develop pharmacological strategies which may also focus on resolution biology.