Most severe cases with COVID-19, especially those with pulmonary failure, are not a consequence of viral burden and/or failure of the ‘adaptive’ immune response to subdue the pathogen by utilizing an adequate ‘adaptive’ immune defense. Rather it is a consequence of immunopathology, resulting from imbalanced innate immune response, which may not be linked to pathogen burden at all. In fact, it might be described as an autoinflammatory disease. The Kawasaki-like disease seen in children with SARS-CoV-2 exposure might be another example of similar mechanism. Highlights • Severe COVID-19 is not a consequence of excessive viral burden • Severe COVID-19 is an autoinflammatory disease • The adaptive immune system is not a defense organization
【저자키워드】 SARS-CoV-2, coronavirus, immune response, Innate immunity, COVID-19, Coronavirus disease 2019, SARS-CoV-2, Severe acute respiratory syndrome coronavirus 2, cytokine, Kawasaki disease, ACE2, angiotensin converting enzyme 2, MERS, Middle East respiratory syndrome, CoV, coronavirus, TLR, Toll-like receptor, CRS, Cytokine release syndrome, NET, neutrophil extracellular trap, SNP, single nucleotide polymorphism, ADE, antibody dependent enhancement, Ab, antibody, ARDS, Acute Respiratory Disease Syndrome, IFN, type I/III interferons, GWAS, genome wide association study,