Elsevier

The Journal of Pediatrics

Volume 227, December 2020, Pages 45-52.e5
The Journal of Pediatrics

Original Article
Pediatric Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2): Clinical Presentation, Infectivity, and Immune Responses

https://doi.org/10.1016/j.jpeds.2020.08.037Get rights and content

Objectives

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.

Study design

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.

Results

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.

Conclusions

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.

Abbreviations

ACE2
Angiotensin-converting enzyme
COVID-19
Coronavirus disease-19
IPO8
Importin-8
IRB
Institutional Review Board
MGH
Massachusetts General Hospital
MIS-C
Multisystem inflammatory syndrome in children
NT-proBNB
N-terminal pro b-type natriuretic peptide
RBD
Receptor binding domain
RSV
Respiratory syncytial virus
SARS-CoV-2
Severe acute respiratory syndrome coronavirus 2

Cited by (0)

Supported by the National Heart, Lung, and Blood Institute (5K08HL143183 to L.Y.), the Cystic Fibrosis Foundation (YONKER18Q0 to L.Y.), the National Institute of Child Health and Human Development (K08 HD094638 [to A.N.] and R01HD100022 [to A.E.]), Mark and Lisa Schwartz (to J.L.), the National Institute of Diabetes and Digestive and Kidney Diseases (DK039773, DK072381 [to J.B.] and DK104344 [to A.F.]), the National Institute of Allergy and Infectious Disease (K24AI141036 to I.B.), the Centers for Disease Control and Prevention (U01CK000490 to E.R.), and the Department of Pediatrics and the Department of Obstetrics/Gynecology at Massachusetts General Hospital (to L.Y. and A.E.). The authors declare no conflicts of interest.

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