ISSN Print 2713-2757
ISSN Online 2713-2765
SCIENTIFIC AND PRACTICAL REVIEWED JOURNAL OF FMBA OF RUSSIA
Copyright: © 2023 by the authors. Licensee: Pirogov University.
This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (CC BY).
This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (CC BY).
REVIEW
Current understanding of epidemiology and pathogenesis of multisystem inflammatory syndrome associated with SARS-CoV-2 in children
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]
