REVIEW

Current understanding of epidemiology and pathogenesis of multisystem inflammatory syndrome associated with SARS-CoV-2 in children

Konstantinova YuE1, Vilnits AA1,2, Bekhtereva MK1,2, Alekseeva LA1, Glotov OS1, Egorova ES1
About authors

1 Pediatric Research and Clinical Center of Infectious Diseases of the Federal Medical Biological Agency, Saint Petersburg, Russia

2 Saint Petersburg State Pediatric Medical University, Saint-Petersburg, Russia

Correspondence should be addressed: Yulia E. Konstantinova
Professora Popova, 9, Saint Petersburg, 197022, Russia; ur.liam@32avonitnatsnok.ailuy

About paper

Author contribution: Konstantinova YuE, Alekseeva LA, Glotov OS, Egorova ES — search for literature, manuscript writing and editing, approval of the final version of the article; Vilnitz AA, Bekhtereva MK — concept development, search for literature, manuscript writing and editing, approval of the final version of the article.

Received: 2023-08-25 Accepted: 2023-09-10 Published online: 2023-09-30
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Fig. 1. Schematic representation of antibody-dependent enhancement: binding of SARS-CoV-2 by non-neutralizing antibodies → presentation of the virus to the cell → virus uptake into the monocyte/macrophage → virus replication in the cell → release of SARS-CoV-2 copies. Adapted from [32]
Fig. 2. Schematic representation of antibody-dependent enhancement: binding of SARS-CoV-2 by non-neutralizing antibodies → immune complexes’ formation and deposition in the tissues → hyperimmune response. Adapted from [32]
Fig. 3. Schematic representation of superantigen theory as MIS-C pathogenesis: SARS-CoV-2 persistence in the gut → zonulin release → disruption of intercellular contacts and increased intestinal permeability → viral S-protein S1 subunit entry in the bloodstream (as superantigen) → bonding of MHC II molecules found on the antigen-presenting cells with S1 subunit of the virus and T cell activation via TCR → hyperimmune response. Modified and adapted from [35, 37]