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.