PMC:7546716 / 1439-2698 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7546716","sourcedb":"PMC","sourceid":"7546716","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7546716","text":"Intensive efforts are underway to unravel the immunopathology of COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and to control the pandemic. Given the public health emergency, scarcity of effective antiviral therapies, and rapid evolution of lung disease associated with COVID-19, patients who are critically ill with COVID-19 and have exuberant inflammation, life-threatening acute respiratory distress syndrome, and coagulopathy, are basically treated as if they had secondary haemophagocytic lymphohistiocytosis or virus-associated macrophage activation syndrome (MAS). These treatments are focused on therapies that neutralise key cytokines driving classical MAS, such as interleukin-6 ([IL]-6; eg, tocilizumab) or interferon gamma (IFNγ; eg, emapalumab).1, 2 In fact, some fatal cases of COVID-19 are accompanied not only by severe respiratory disease, but also by increased systemic inflammation as shown by higher ferritin concentrations.2 However, in many aspects, COVID-19 does not resemble typical MAS. We propose that the cytokine storm syndrome seen in COVID-19 is dissimilar to that seen in canonical MAS and should be regarded as a distinct entity and approached in a novel way reflecting its unique 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