COVID-19 and multisystem inflammatory syndrome in children and adolescents

Jiang, Li; Tang, Kun; Levin, Michael; Irfan, Omar; Morris, Shaun; Wilson, Karen M.; Klein, Jonathan D.; Bhutta, Zulfiqar A

doi:10.1016/s1473-3099(20)30651-4

Cited by 719 publications

(996 citation statements)

References 113 publications

(231 reference statements)

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“…Delayed clearance of the SARS-CoV-2 leading to unchecked inflammation is a possible mechanism of disease for PIMS-TS (Fig. 1C) [8]. Certainly, children with PIMS-TS have greatly elevated serum concentrations of pro-inflammatory interleukins (IL-1 beta, IL-17, IL-6 and IL-8), accompanied by activation of neutrophils and monocytes [9].…”

Section: What Is the Pathobiology Of Pims-ts?mentioning

confidence: 99%

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Paediatric Inflammatory Multisystem Syndrome Temporally-Associated with SARS-CoV-2 Infection: An Overview

2020

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In spring 2020 paediatricians working across Europe and the USA [1] alerted colleagues to clusters of previously healthy children presenting with unremitting fever, multisystem inflammation and pancarditis. This syndrome, initially termed Inflammatory Multisystem Syndrome Temporally Associated with SARS-CoV-2 infection (PIMS-TS), or by its US variation Multisystem Inflammatory Syndrome in Children (MIS-C; Table 1), appears to be a rare complication of (largely) asymptomatic SARS-CoV-2 infection in children [8]. However, the overlap with other paediatric inflammatory syndromes such as Kawasaki disease (KD) and optimum treatments remain unknown. We provide a narrative overview of PIMS-TS and highlight important knowledge gaps.

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Section: What Is the Pathobiology Of Pims-ts?mentioning

confidence: 99%

“…Important questions remain [8]: How to tease out environmental, genetic and acquired risk factors for PIMS-TS? What are the long-term outcomes of children with PIMS-TS?…”

Section: Into the Unknown; Againmentioning

confidence: 99%

Paediatric Inflammatory Multisystem Syndrome Temporally-Associated with SARS-CoV-2 Infection: An Overview

2020

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“…Importantly, SARS-CoV2 presence is associated with pathologic profile. The inflammatory illness in children is consistent with the vascular cell target of SARS-CoV2 (50). SARS2-CoV2 infection in children results in autoimmune and autoinflammatory responses that are termed as pediatric inflammatory multisystem syndrome (PIMS) or multisystem inflammatory syndrome in children (MISC-C) (45,51,52).…”

Section: Socs1/3 Antagonist and Severe Covid-19mentioning

confidence: 83%

SOCS, Intrinsic Virulence Factors, and Treatment of COVID-19

2020

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The suppressor of cytokine signaling (SOCS) family of intracellular checkpoint inhibitors has received little recognition compared to other checkpoint inhibitors. Two members of this family, SOCS1 and SOCS3, are indispensable, since SOCS1 knockout in mice results in neonatal death due to interferon gamma (IFNg) induced inflammatory disease, and SOCS3 knockout leads to embryonic lethality. We have shown that SOCS1 and SOCS3 (SOCS1/3) function as virus induced intrinsic virulence factors for influenza A virus, EMC virus, herpes simplex virus 1 (HSV-1), and vaccinia virus infections. Other viruses such as pathogenic pig enteric coronavirus and coronavirus induced severe acute respiratory syndrome (SARS) spike protein also induce SOCS virus intrinsic virulence factors. SOCS1/3 exert their viral virulence effect via inhibition of type I and type II interferon (IFN) function. Specifically, the SOCS bind to the activation loop of receptor-associated tyrosine kinases JAK2 and TYK2 through the SOCS kinase inhibitory region (KIR), which inhibits STAT transcription factor activation by the kinases. Activated STATs are required for IFN function. We have developed a small peptide antagonist of SOCS1/3 that blocks SOCS1/3 inhibitory activity and prevents virus pathogenesis. The antagonist, pJAK2 (1001-1013), is comprised of the JAK2 activation loop, phosphorylated at tyrosine 1007 with a palmitate for cell penetration. The remarkable thing about SOCS1/3 is that it serves as a broad, simple tool of perhaps most pathogenic viruses to avoid innate host IFN defense. We suggest in this Perspective that SOCS1/3 antagonist is a simple counter measure to SOCS1/3 and should be an effective mechanism as a prophylactic and/or therapeutic against the COVID-19 pandemic that is caused by coronavirus SARS-CoV2.

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“…antibody-dependent enhancement (ADE), direct cytotoxicity, immune complexes, and macrophage hyperinflammatory responses, 33 perhaps enabled by substantial differences in humoral responses. 7 Another theoretical possibility would be innate activities of anti-RBD antibodies.…”

Section: How Could Aberrant Immune Responses Promote Mis-c? Hypothetimentioning

confidence: 99%

Multisystem Inflammatory Syndrome in Children and SARS-CoV-2 Serology

Zeichner

Cruz

2020

Pediatrics

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This is a prepublication version of an article that has undergone peer review and been accepted for publication but is not the final version of record. This paper may be cited using the DOI and date of access. This paper may contain information that has errors in facts, figures, and statements, and will be corrected in the final published version. The journal is providing an early version of this article to expedite access to this information. The American Academy of Pediatrics, the editors, and authors are not responsible for inaccurate information and data described in this version.

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COVID-19 and multisystem inflammatory syndrome in children and adolescents

Cited by 719 publications

References 113 publications

Paediatric Inflammatory Multisystem Syndrome Temporally-Associated with SARS-CoV-2 Infection: An Overview

Paediatric Inflammatory Multisystem Syndrome Temporally-Associated with SARS-CoV-2 Infection: An Overview

SOCS, Intrinsic Virulence Factors, and Treatment of COVID-19

Multisystem Inflammatory Syndrome in Children and SARS-CoV-2 Serology

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