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.⁹, Elsevier.