Understanding SARS-CoV-2-related multisystem inflammatory syndrome in children - PubMed (original) (raw)

Review

Anne H Rowley. Nat Rev Immunol. 2020 Aug.

Abstract

A new multisystem inflammatory syndrome apparently related to infection with SARS-CoV-2 has recently been reported in older children (known as MIS-C), manifested by severe abdominal pain, cardiac dysfunction and shock. Here, I discuss the similarities and differences between MIS-C and Kawasaki disease, focusing on their epidemiology, aetiology and pathophysiological mechanisms.

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Conflict of interest statement

A.H.R. is a named investigator on National Institutes of Health R21AI140029 and Provisional Patent 62/811,930 on Antibodies and Antigens of Kawasaki disease.

Figures

Fig. 1

Fig. 1. Pathogenesis of multisystem inflammatory syndrome in children: a hypothesis.

The timing of the interferon (IFN) response to SARS-CoV-2 infection can vary with viral load and genetic differences in host response. When viral load is low, IFN responses are engaged and contribute to viral clearance, resulting in mild infection. When viral load is high and/or genetic factors slow antiviral responses, virus replication can delay the IFN response and cytokine storm can result before adaptive responses clear the virus, resulting in severe disease including multisystem inflammatory syndrome in children (MIS-C). Adapted with permission from REF., Elsevier.

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