Thromboinflammation in coronavirus disease 2019: The clot thickens

Since the start of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, a disease that has become one of the world's greatest global health challenges, the role of the immune system has been at the forefront of scientific studies. The pathophysiology of coronavirus disease 2019 (COVID-19) is complex, which is evident in those at higher risk for poor outcome. Multiple systems contribute to thrombosis and inflammation seen in COVID-19 patients, including neutrophil and platelet activation, and endothelial dysfunction. Understanding how the immune system functions in different patient cohorts (particularly given recent emerging events with the Oxford/AstraZeneca vaccine) is vital to understanding the pathophysiology of this devastating disease and for the subsequent development of novel therapeutic targets and to facilitate possible drug repurposing strategies that could benefit society on a global scale.

Automated summary

The pathophysiology of COVID-19 is complex, with multiple systems contributing to thrombosis and inflammation. Understanding the role of the immune system in different patient cohorts is crucial for developing novel therapeutic targets and drug repurposing strategies.