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Review
. 2020 Nov:220:108588.
doi: 10.1016/j.clim.2020.108588. Epub 2020 Sep 6.

SARS-CoV-2 infections in children and young people

Affiliations
Review

SARS-CoV-2 infections in children and young people

Susanna Felsenstein et al. Clin Immunol. 2020 Nov.

Abstract

Though recent reports link SARS-CoV-2 infections with hyper-inflammatory states in children, most children experience no/mild symptoms, and hospitalization and mortality rates are low in the age group. As symptoms are usually mild and seroconversion occurs at low frequencies, it remains unclear whether children significantly contribute to community transmission. Several hypotheses try to explain age-related differences in disease presentation and severity. Possible reasons for milder presentations in children as compared to adults include frequent contact to seasonal coronaviruses, presence of cross-reactive antibodies, and/or co-clearance with other viruses. Increased expression of ACE2 in young people may facilitate virus infection, while limiting inflammation and reducing the risk of severe disease. Further potential factors include recent vaccinations and a more diverse memory T cell repertoire. This manuscript reviews age-related host factors that may protect children from COVID-19 and complications associated, and addresses the confusion around seropositivity and immunity.

Keywords: COVID; Children; Inflammation; MIS-C; PIMS-TS; Pathology; SARS-CoV-2; Treatment.

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Figures

Fig. 1
Fig. 1
Immune pathogenesis of COVID-19. SARS-CoV2 can infect epithelial cells (EC) through the ACE2 transmembrane enzyme. It evades the early innate immune response through suppressing Toll-like receptor (TLR3 and 7) and/or cytosolic RNA receptor (RIG-I, MDA5) mediated type I interferon signaling, which results in spreading of the infection. When a threshold is reached, cells become necrotic and virus particles are released together with nuclear and cytosolic components, both of which can form immune complexes. Virus containing IC infect monocytes/macrophages (Mφ) and induce massive pro-inflammatory cytokine expression (IL-1, IL-6, TNF-α) in a process named antibody dependent enhancement. IC also activate the complement and clotting cascades, contributing to inflammation and deranged coagulation. Further (uninfected) monocytes/macrophages invade the area and produce type I interferons and pro-inflammatory cytokines, further contributing to inflammation and tissue damage.

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