Pediatric Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2): Clinical Presentation, Infectivity, and Immune Responses
As schools plan for re-opening, understanding the potential role children play in the coronavirus infectious disease 2019 (COVID-19) pandemic and the factors that drive severe illness in children is critical. Children ages 0-22 years with suspected severe acute respiratory syndrome coronavirus 2 (SA...
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Published in | The Journal of pediatrics Vol. 227; pp. 45 - 52.e5 |
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Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.12.2020
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Subjects | |
Online Access | Get full text |
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Abstract | As schools plan for re-opening, understanding the potential role children play in the coronavirus infectious disease 2019 (COVID-19) pandemic and the factors that drive severe illness in children is critical.
Children ages 0-22 years with suspected severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection presenting to urgent care clinics or being hospitalized for confirmed/suspected SARS-CoV-2 infection or multisystem inflammatory syndrome in children (MIS-C) at Massachusetts General Hospital were offered enrollment in the Massachusetts General Hospital Pediatric COVID-19 Biorepository. Enrolled children provided nasopharyngeal, oropharyngeal, and/or blood specimens. SARS-CoV-2 viral load, ACE2 RNA levels, and serology for SARS-CoV-2 were quantified.
A total of 192 children (mean age, 10.2 ± 7.0 years) were enrolled. Forty-nine children (26%) were diagnosed with acute SARS-CoV-2 infection; an additional 18 children (9%) met the criteria for MIS-C. Only 25 children (51%) with acute SARS-CoV-2 infection presented with fever; symptoms of SARS-CoV-2 infection, if present, were nonspecific. Nasopharyngeal viral load was highest in children in the first 2 days of symptoms, significantly higher than hospitalized adults with severe disease (P = .002). Age did not impact viral load, but younger children had lower angiotensin-converting enzyme 2 expression (P = .004). Immunoglobulin M (IgM) and Immunoglobulin G (IgG) to the receptor binding domain of the SARS-CoV-2 spike protein were increased in severe MIS-C (P < .001), with dysregulated humoral responses observed.
This study reveals that children may be a potential source of contagion in the SARS-CoV-2 pandemic despite having milder disease or a lack of symptoms; immune dysregulation is implicated in severe postinfectious MIS-C. |
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AbstractList | As schools plan for re-opening, understanding the potential role children play in the coronavirus infectious disease 2019 (COVID-19) pandemic and the factors that drive severe illness in children is critical.OBJECTIVESAs schools plan for re-opening, understanding the potential role children play in the coronavirus infectious disease 2019 (COVID-19) pandemic and the factors that drive severe illness in children is critical.Children ages 0-22 years with suspected severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection presenting to urgent care clinics or being hospitalized for confirmed/suspected SARS-CoV-2 infection or multisystem inflammatory syndrome in children (MIS-C) at Massachusetts General Hospital were offered enrollment in the Massachusetts General Hospital Pediatric COVID-19 Biorepository. Enrolled children provided nasopharyngeal, oropharyngeal, and/or blood specimens. SARS-CoV-2 viral load, ACE2 RNA levels, and serology for SARS-CoV-2 were quantified.STUDY DESIGNChildren ages 0-22 years with suspected severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection presenting to urgent care clinics or being hospitalized for confirmed/suspected SARS-CoV-2 infection or multisystem inflammatory syndrome in children (MIS-C) at Massachusetts General Hospital were offered enrollment in the Massachusetts General Hospital Pediatric COVID-19 Biorepository. Enrolled children provided nasopharyngeal, oropharyngeal, and/or blood specimens. SARS-CoV-2 viral load, ACE2 RNA levels, and serology for SARS-CoV-2 were quantified.A total of 192 children (mean age, 10.2 ± 7.0 years) were enrolled. Forty-nine children (26%) were diagnosed with acute SARS-CoV-2 infection; an additional 18 children (9%) met the criteria for MIS-C. Only 25 children (51%) with acute SARS-CoV-2 infection presented with fever; symptoms of SARS-CoV-2 infection, if present, were nonspecific. Nasopharyngeal viral load was highest in children in the first 2 days of symptoms, significantly higher than hospitalized adults with severe disease (P = .002). Age did not impact viral load, but younger children had lower angiotensin-converting enzyme 2 expression (P = .004). Immunoglobulin M (IgM) and Immunoglobulin G (IgG) to the receptor binding domain of the SARS-CoV-2 spike protein were increased in severe MIS-C (P < .001), with dysregulated humoral responses observed.RESULTSA total of 192 children (mean age, 10.2 ± 7.0 years) were enrolled. Forty-nine children (26%) were diagnosed with acute SARS-CoV-2 infection; an additional 18 children (9%) met the criteria for MIS-C. Only 25 children (51%) with acute SARS-CoV-2 infection presented with fever; symptoms of SARS-CoV-2 infection, if present, were nonspecific. Nasopharyngeal viral load was highest in children in the first 2 days of symptoms, significantly higher than hospitalized adults with severe disease (P = .002). Age did not impact viral load, but younger children had lower angiotensin-converting enzyme 2 expression (P = .004). Immunoglobulin M (IgM) and Immunoglobulin G (IgG) to the receptor binding domain of the SARS-CoV-2 spike protein were increased in severe MIS-C (P < .001), with dysregulated humoral responses observed.This study reveals that children may be a potential source of contagion in the SARS-CoV-2 pandemic despite having milder disease or a lack of symptoms; immune dysregulation is implicated in severe postinfectious MIS-C.CONCLUSIONSThis study reveals that children may be a potential source of contagion in the SARS-CoV-2 pandemic despite having milder disease or a lack of symptoms; immune dysregulation is implicated in severe postinfectious MIS-C. As schools plan for re-opening, understanding the potential role children play in the coronavirus infectious disease 2019 (COVID-19) pandemic and the factors that drive severe illness in children is critical. Children ages 0-22 years with suspected severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection presenting to urgent care clinics or being hospitalized for confirmed/suspected SARS-CoV-2 infection or multisystem inflammatory syndrome in children (MIS-C) at Massachusetts General Hospital were offered enrollment in the Massachusetts General Hospital Pediatric COVID-19 Biorepository. Enrolled children provided nasopharyngeal, oropharyngeal, and/or blood specimens. SARS-CoV-2 viral load, ACE2 RNA levels, and serology for SARS-CoV-2 were quantified. A total of 192 children (mean age, 10.2 ± 7.0 years) were enrolled. Forty-nine children (26%) were diagnosed with acute SARS-CoV-2 infection; an additional 18 children (9%) met the criteria for MIS-C. Only 25 children (51%) with acute SARS-CoV-2 infection presented with fever; symptoms of SARS-CoV-2 infection, if present, were nonspecific. Nasopharyngeal viral load was highest in children in the first 2 days of symptoms, significantly higher than hospitalized adults with severe disease (P = .002). Age did not impact viral load, but younger children had lower angiotensin-converting enzyme 2 expression (P = .004). Immunoglobulin M (IgM) and Immunoglobulin G (IgG) to the receptor binding domain of the SARS-CoV-2 spike protein were increased in severe MIS-C (P < .001), with dysregulated humoral responses observed. This study reveals that children may be a potential source of contagion in the SARS-CoV-2 pandemic despite having milder disease or a lack of symptoms; immune dysregulation is implicated in severe postinfectious MIS-C. |
Author | Fialkowski, Allison Appleman, Lori Bassett, Ingrid V. Patel, Ankit B. Arya, Puneeta Irimia, Daniel Lerou, Paul H. Bartsch, Yannic Hardcastle, Margot D'Avino, Paolo Edlow, Andrea G. St. John, Anita Lima, Rosiane Bonventre, Joseph V. Yu, Xu G. Alter, Galit Yockey, Laura J. Fischinger, Stephanie Fasano, Alessio Regan, James Yonker, Lael M. Ryan, Edward T. Neilan, Anne M. Chiu, Michelle L. Bordt, Evan A. Park, Grace Shui, Jessica E. Gootkind, Elizabeth De la Flor, Denis Li, Jonathan Z. |
Author_xml | – sequence: 1 givenname: Lael M. surname: Yonker fullname: Yonker, Lael M. email: lyonker@mgh.harvard.edu organization: Mucosal Immunology and Biology Research Center, Massachusetts General Hospital, Boston, MA – sequence: 2 givenname: Anne M. surname: Neilan fullname: Neilan, Anne M. organization: Department of Pediatrics, Massachusetts General Hospital, Boston, MA – sequence: 3 givenname: Yannic surname: Bartsch fullname: Bartsch, Yannic organization: Harvard Medical School, Boston, MA – sequence: 4 givenname: Ankit B. surname: Patel fullname: Patel, Ankit B. organization: Harvard Medical School, Boston, MA – sequence: 5 givenname: James orcidid: 0000-0003-0449-2295 surname: Regan fullname: Regan, James organization: Department of Infectious Diseases, Brigham and Women's Hospital, Boston, MA – sequence: 6 givenname: Puneeta surname: Arya fullname: Arya, Puneeta organization: Department of Pediatrics, Massachusetts General Hospital, Boston, MA – sequence: 7 givenname: Elizabeth surname: Gootkind fullname: Gootkind, Elizabeth organization: Department of Pediatrics, Massachusetts General Hospital, Boston, MA – sequence: 8 givenname: Grace surname: Park fullname: Park, Grace organization: Department of Pediatrics, Massachusetts General Hospital, Boston, MA – sequence: 9 givenname: Margot surname: Hardcastle fullname: Hardcastle, Margot organization: Department of Pediatrics, Massachusetts General Hospital, Boston, MA – sequence: 10 givenname: Anita surname: St. John fullname: St. John, Anita organization: Department of Pediatrics, Massachusetts General Hospital, Boston, MA – sequence: 11 givenname: Lori surname: Appleman fullname: Appleman, Lori organization: Department of Pediatrics, Massachusetts General Hospital, Boston, MA – sequence: 12 givenname: Michelle L. surname: Chiu fullname: Chiu, Michelle L. organization: Department of Pediatrics, Massachusetts General Hospital, Boston, MA – sequence: 13 givenname: Allison surname: Fialkowski fullname: Fialkowski, Allison organization: Harvard Medical School, Boston, MA – sequence: 14 givenname: Denis surname: De la Flor fullname: De la Flor, Denis organization: Mucosal Immunology and Biology Research Center, Massachusetts General Hospital, Boston, MA – sequence: 15 givenname: Rosiane surname: Lima fullname: Lima, Rosiane organization: Mucosal Immunology and Biology Research Center, Massachusetts General Hospital, Boston, MA – sequence: 16 givenname: Evan A. surname: Bordt fullname: Bordt, Evan A. organization: Department of Pediatrics, Massachusetts General Hospital, Boston, MA – sequence: 17 givenname: Laura J. surname: Yockey fullname: Yockey, Laura J. organization: Department of Internal Medicine, Massachusetts General Hospital, Boston, MA – sequence: 18 givenname: Paolo surname: D'Avino fullname: D'Avino, Paolo organization: Mucosal Immunology and Biology Research Center, Massachusetts General Hospital, Boston, MA – sequence: 19 givenname: Stephanie surname: Fischinger fullname: Fischinger, Stephanie organization: Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard, Harvard Medical School, Cambridge, MA – sequence: 20 givenname: Jessica E. surname: Shui fullname: Shui, Jessica E. organization: Department of Pediatrics, Massachusetts General Hospital, Boston, MA – sequence: 21 givenname: Paul H. surname: Lerou fullname: Lerou, Paul H. organization: Department of Pediatrics, Massachusetts General Hospital, Boston, MA – sequence: 22 givenname: Joseph V. surname: Bonventre fullname: Bonventre, Joseph V. organization: Harvard Medical School, Boston, MA – sequence: 23 givenname: Xu G. surname: Yu fullname: Yu, Xu G. organization: Harvard Medical School, Boston, MA – sequence: 24 givenname: Edward T. surname: Ryan fullname: Ryan, Edward T. organization: Department of Pediatrics, Massachusetts General Hospital, Boston, MA – sequence: 25 givenname: Ingrid V. surname: Bassett fullname: Bassett, Ingrid V. organization: Harvard Medical School, Boston, MA – sequence: 26 givenname: Daniel surname: Irimia fullname: Irimia, Daniel organization: Harvard Medical School, Boston, MA – sequence: 27 givenname: Andrea G. surname: Edlow fullname: Edlow, Andrea G. organization: Harvard Medical School, Boston, MA – sequence: 28 givenname: Galit surname: Alter fullname: Alter, Galit organization: Harvard Medical School, Boston, MA – sequence: 29 givenname: Jonathan Z. surname: Li fullname: Li, Jonathan Z. organization: Harvard Medical School, Boston, MA – sequence: 30 givenname: Alessio surname: Fasano fullname: Fasano, Alessio organization: Mucosal Immunology and Biology Research Center, Massachusetts General Hospital, Boston, MA |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32827525$$D View this record in MEDLINE/PubMed |
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ContentType | Journal Article |
Copyright | 2020 Elsevier Inc. Copyright © 2020 Elsevier Inc. All rights reserved. 2020 Elsevier Inc. All rights reserved. 2020 Elsevier Inc. |
Copyright_xml | – notice: 2020 Elsevier Inc. – notice: Copyright © 2020 Elsevier Inc. All rights reserved. – notice: 2020 Elsevier Inc. All rights reserved. 2020 Elsevier Inc. |
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Title | Pediatric Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2): Clinical Presentation, Infectivity, and Immune Responses |
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