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Review
. 2020 Dec 1;130(12):6194-6197.
doi: 10.1172/JCI145301.

Inflammatory syndromes associated with SARS-CoV-2 infection: dysregulation of the immune response across the age spectrum

Jill E Weatherhead  1   2   3 , Eva Clark  1   3   4 , Tiphanie P Vogel  5   6 , Robert L Atmar  1 , Prathit A Kulkarni  1   7
Affiliations
Review

Inflammatory syndromes associated with SARS-CoV-2 infection: dysregulation of the immune response across the age spectrum

Jill E Weatherhead et al. J Clin Invest. .
No abstract available

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Conflict of interest statement

Conflict of interest: The authors have declared that no conflict of interest exists.

Figures

Figure 1
Figure 1. Potential mechanisms for inflammatory syndromes associated with SARS-CoV-2.
SARS-CoV-2 can trigger a range of inflammatory syndromes across the age spectrum. Compared with children, adults — particularly those with certain preexisting proinflammatory comorbidities — are more likely to develop acute COVID-19–associated hyperinflammatory syndrome within 1 to 2 weeks of exposure to SARS-CoV-2. COVID-19–associated hyperinflammatory syndrome begins with failure of the regulatory immune response to SARS-CoV-2, including abnormal interferon production that drives macrophage hyperactivation. This results in inflammatory cytokine cascades and causes significant damage to multiple organ systems. In contrast, children are more likely to have asymptomatic or mild acute SARS-CoV-2 infection without sequelae. The reason or reasons why children do not commonly develop acute COVID-19–associated hyperinflammatory syndrome remain unknown. However, both children and adults can develop MIS-C/A of unclear etiology weeks after initial asymptomatic or mild SARS-CoV-2 infection. The precise cause of MIS-C/A inflammatory symptoms remains unclear, but may be due to development of abnormal antibody responses that drive systemic hyperinflammation. APC, antigen-presenting cell; ESR, erythrocyte sedimentation rate; LDH, lactate dehydrogenase; ALC, absolute lymphocyte count; GCSF, granulocyte colony-stimulating factor; IP-10, interferon-γ–induced protein–10; MCP1, monocyte chemotactic protein 1; MIP1α, macrophage inflammatory protein 1α; BNP, brain natriuretic peptide.
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References

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Publication types

Supplementary concepts