Immunological Assessment of Pediatric Multisystem Inflammatory Syndrome Related to Coronavirus Disease 2019.

SARS-CoV-2 immunological and virological workup multisystem inflammatory syndrome in children

Journal

Journal of the Pediatric Infectious Diseases Society
ISSN: 2048-7207
Titre abrégé: J Pediatric Infect Dis Soc
Pays: England
ID NLM: 101586049

Informations de publication

Date de publication:
14 Aug 2021
Historique:
received: 03 07 2020
accepted: 10 11 2020
pubmed: 13 11 2020
medline: 18 8 2021
entrez: 12 11 2020
Statut: ppublish

Résumé

Recently, cases of multisystem inflammatory syndrome in children (MIS-C) associated with coronavirus disease 2019 (COVID-19) have been reported worldwide. Negative polymerase chain reaction (RT-PCR) testing associated with positive serology in most of the cases suggests a postinfectious syndrome. Because the pathophysiology of this syndrome is still poorly understood, extensive virological and immunological investigations are needed. We report a series of 4 pediatric patients admitted to Geneva University Hospitals with persistent fever and laboratory evidence of inflammation meeting the published definition of MIS-C related to COVID-19, to whom an extensive virological and immunological workup was performed. RT-PCRs on multiple anatomical compartments were negative, whereas anti-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) immunoglobulin A (IgA) and immunoglobulin G (IgG) were strongly positive by enzyme-linked immunosorbent assay and immunofluorescence. Both pseudoneutralization and full virus neutralization assays showed the presence of neutralizing antibodies in all children, confirming a recent infection with SARS-CoV-2. The analyses of cytokine profiles revealed an elevation in all cytokines, as reported in adults with severe COVID-19. Although differing in clinical presentation, some features of MIS-C show phenotypic overlap with hemophagocytic lymphohistiocytosis (HLH). In contrast to patients with primary HLH, our patients showed normal perforin expression and natural killer (NK) cell degranulation. The levels of soluble interleukin (IL)-2 receptor (sIL-2R) correlated with the severity of disease, reflecting recent T-cell activation. Our findings suggest that MIS-C related to COVID-19 is caused by a postinfectious inflammatory syndrome associated with an elevation in all cytokines, and markers of recent T-cell activation (sIL-2R) occurring despite a strong and specific humoral response to SARS-CoV-2. Further functional and genetic analyses are essential to better understand the mechanisms of host-pathogen interactions.

Sections du résumé

BACKGROUND BACKGROUND
Recently, cases of multisystem inflammatory syndrome in children (MIS-C) associated with coronavirus disease 2019 (COVID-19) have been reported worldwide. Negative polymerase chain reaction (RT-PCR) testing associated with positive serology in most of the cases suggests a postinfectious syndrome. Because the pathophysiology of this syndrome is still poorly understood, extensive virological and immunological investigations are needed.
METHODS METHODS
We report a series of 4 pediatric patients admitted to Geneva University Hospitals with persistent fever and laboratory evidence of inflammation meeting the published definition of MIS-C related to COVID-19, to whom an extensive virological and immunological workup was performed.
RESULTS RESULTS
RT-PCRs on multiple anatomical compartments were negative, whereas anti-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) immunoglobulin A (IgA) and immunoglobulin G (IgG) were strongly positive by enzyme-linked immunosorbent assay and immunofluorescence. Both pseudoneutralization and full virus neutralization assays showed the presence of neutralizing antibodies in all children, confirming a recent infection with SARS-CoV-2. The analyses of cytokine profiles revealed an elevation in all cytokines, as reported in adults with severe COVID-19. Although differing in clinical presentation, some features of MIS-C show phenotypic overlap with hemophagocytic lymphohistiocytosis (HLH). In contrast to patients with primary HLH, our patients showed normal perforin expression and natural killer (NK) cell degranulation. The levels of soluble interleukin (IL)-2 receptor (sIL-2R) correlated with the severity of disease, reflecting recent T-cell activation.
CONCLUSION CONCLUSIONS
Our findings suggest that MIS-C related to COVID-19 is caused by a postinfectious inflammatory syndrome associated with an elevation in all cytokines, and markers of recent T-cell activation (sIL-2R) occurring despite a strong and specific humoral response to SARS-CoV-2. Further functional and genetic analyses are essential to better understand the mechanisms of host-pathogen interactions.

Identifiants

pubmed: 33180935
pii: 5979492
doi: 10.1093/jpids/piaa142
pmc: PMC7717282
doi:

Substances chimiques

Antibodies, Neutralizing 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

706-713

Subventions

Organisme : Beatrice Ederer Weber Foundation

Informations de copyright

© The Author(s) 2020. Published by Oxford University Press on behalf of The Journal of the Pediatric Infectious Diseases Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Auteurs

Serge Grazioli (S)

Division of Neonatal and Pediatric Intensive Care, Faculty of Medicine, Geneva University Hospitals, Geneva, Switzerland.

Fedora Tavaglione (F)

Division of Neonatal and Pediatric Intensive Care, Faculty of Medicine, Geneva University Hospitals, Geneva, Switzerland.

Giulia Torriani (G)

Geneva Centre for Emerging Viral Diseases, Geneva University Hospitals and Faculty of Medicine, Geneva Switzerland.

Noemie Wagner (N)

Pediatric Infectious Diseases Unit, Faculty of Medicine, Geneva University Hospitals, Geneva, Switzerland.

Marie Rohr (M)

Pediatric Infectious Diseases Unit, Faculty of Medicine, Geneva University Hospitals, Geneva, Switzerland.

Arnaud G L'Huillier (AG)

Geneva Centre for Emerging Viral Diseases, Geneva University Hospitals and Faculty of Medicine, Geneva Switzerland.
Pediatric Infectious Diseases Unit, Faculty of Medicine, Geneva University Hospitals, Geneva, Switzerland.

Charlotte Leclercq (C)

Children's Hospital of Geneva, Faculty of Medicine, Geneva University Hospitals, Geneva, Switzerland.

Anne Perrin (A)

Children's Hospital of Geneva, Faculty of Medicine, Geneva University Hospitals, Geneva, Switzerland.

Alice Bordessoule (A)

Division of Neonatal and Pediatric Intensive Care, Faculty of Medicine, Geneva University Hospitals, Geneva, Switzerland.

Maurice Beghetti (M)

Pediatric Cardiology Unit, Children's Hospital of Geneva, Faculty of Medicine, Geneva University Hospitals, Geneva, Switzerland.

Jana Pachlopnik Schmid (JP)

Children's Hospital of Zurich, Zurich, Switzerland.

Stefano Vavassori (S)

Children's Hospital of Zurich, Zurich, Switzerland.

Matthieu Perreau (M)

Division of Immunology and Allergy, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.

Christiane Eberhardt (C)

Center of Vaccinology, Geneva University Hospitals, Geneva, Switzerland.

Arnaud Didierlaurent (A)

Center of Vaccinology, Geneva University Hospitals, Geneva, Switzerland.

Laurent Kaiser (L)

Geneva Centre for Emerging Viral Diseases, Geneva University Hospitals and Faculty of Medicine, Geneva Switzerland.

Isabella Eckerle (I)

Geneva Centre for Emerging Viral Diseases, Geneva University Hospitals and Faculty of Medicine, Geneva Switzerland.

Pascale Roux-Lombard (P)

Laboratory of Immunology and Allergology, Geneva University Hospitals, Geneva University, Geneva, Switzerland.

Geraldine Blanchard-Rohner (G)

Center of Vaccinology, Geneva University Hospitals, Geneva, Switzerland.
Pediatric Immunology and Vaccinology Unit, Children's Hospital of Geneva, Geneva University Hospitals and Faculty of Medicine, Geneva, Switzerland.

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