Researchers unravel mechanisms that can trigger platelets to cause severe COVID-19 immune response

A medical image shows blood clotting with a virus in the background.

Inflammation and blood clotting are distinct features of severe COVID-19 cases, but understanding single and multifactored mechanisms that activate, drive, and sustain these processes remains a focus of ongoing research. A study in Science Advances expands this knowledge by explaining genes and pathways that can be activated in platelets following exposure to the coronavirus, which can then trigger a hyperinflammatory immune response.  
Researchers identified these patterns after studying biomarkers in blood samples from nearly 300 patients who were hospitalized for COVID-19 and compared these outcomes to cell and laboratory models. The dynamic they observed is characteristic of severe COVID-19 outcomes, including sustained inflammation and blood clotting. The authors cite an ongoing trial that is examining the potential benefits of inhibiting these pathways by providing platelet therapy to hospitalized patients.  

The study was partially supported by the NHLBI, the National Institute of General Medical Sciences, the National Center for Advancing Translational Sciences, and the National Cancer Institute.