Abstract
During the COVID-19 pandemic, children have had markedly different clinical presentations and outcomes compared to adults. In the acute phase of infection, younger children are relatively spared the severe consequences reported in adults. Yet, they are uniquely susceptible to the newly described Multisystem Inflammatory Syndrome in Children (MIS-C). This may result from the developmental “immunodeficiency” resulting from a Th2 polarization that starts in utero and is maintained for most of the first decade of life. MIS-C may be due to IgA complexes in a Th2 environment or a Th1-like response to COVID-19 antigens that developed slowly. Alternatively, MIS-C may occur in vulnerable hosts with genetic susceptibilities in other immune and non-immune pathways. Herein, we present a brief overview of the host immune response, virologic and genetic factors, and comparable inflammatory syndromes that may explain the pathophysiology leading to drastic differences in clinical presentation and outcomes of COVID-19 between children and adults.
Highlights
SARS-CoV-2, a novel coronavirus, was first reported in December 2019 from Wuhan, China
COVID-19 infection in children is markedly different from adults in a number of ways, including differences in transmission itself, as well as differences in severity and pathogenesis including viral genetic diversity, sex-related-impacted protease and viral susceptibility differences, and age-related and potentially genetic innate and adaptive immune response differences
Parallels to other hyperinflammatory syndromes and comparisons in the context of some of these factors may continue to lead to understanding pediatric susceptibility to COVID-19 disease and its associated syndromes
Summary
SARS-CoV-2, a novel coronavirus, was first reported in December 2019 from Wuhan, China. The disease caused by SARS-CoV-2, COVID-19, subsequently spread in pandemic fashion over the following 10 months causing a wide spectrum of clinical symptoms from asymptomatic disease to death [1]. An initial report of a Chinese cohort of 36 children with documented COVID-19 infection revealed relatively mild symptoms [4]. A larger cohort of 110 children documented mostly asymptomatic infection with a shorter duration of viral detection (11 vs 17 days). These early reports indicated that symptomatic children were more likely to have fever, pneumonia, and lymphopenia [5]. This report attempts to apply our knowledge of virology, developmental immunology, comparable inflammatory syndromes, and host genetics to explain the drastic differences in clinical presentation and outcomes between children and adults
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