Abstract

A pathological, dysregulated immune response (ie, hyperinflammation) is a recognised complication of COVID-19.1 The protype hyperinflammatory syndrome secondary to infection is secondary haemophagocytic lymphohistiocytosis (sHLH), but the dominant hyperinflammatory phenotype in people with severe COVID-19-associated pneumonia is not that of sHLH and is poorly understood.1,2 The COVID-19 hyperinflammation phenotype is associated with increased concentrations of inflammatory markers, increased risk of mortality, and subsequent development of immunothrombosis.

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