Abstract
Most severe cases with COVID-19, especially those with pulmonary failure, are not a consequence of viral burden and/or failure of the 'adaptive' immune response to subdue the pathogen by utilizing an adequate 'adaptive' immune defense. Rather it is a consequence of immunopathology, resulting from imbalanced innate immune response, which may not be linked to pathogen burden at all. In fact, it might be described as an autoinflammatory disease. The Kawasaki-like disease seen in children with SARS-CoV-2 exposure might be another example of similar mechanism.
Keywords:
Coronavirus; Cytokine; Immune response; Innate immunity; Kawasaki disease; SARS-CoV-2.
Copyright © 2020 Elsevier Inc. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Acute Disease
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Adaptive Immunity
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Autoimmunity / genetics*
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Betacoronavirus / immunology
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Betacoronavirus / pathogenicity*
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CD4-Positive T-Lymphocytes / immunology
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CD4-Positive T-Lymphocytes / pathology
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CD4-Positive T-Lymphocytes / virology
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CD8-Positive T-Lymphocytes / immunology
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CD8-Positive T-Lymphocytes / pathology
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CD8-Positive T-Lymphocytes / virology
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COVID-19
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Coronavirus Infections / genetics
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Coronavirus Infections / immunology*
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Coronavirus Infections / physiopathology
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Cytokine Release Syndrome / genetics
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Cytokine Release Syndrome / immunology*
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Cytokine Release Syndrome / physiopathology
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Host-Pathogen Interactions / genetics
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Host-Pathogen Interactions / immunology*
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Humans
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Immunity, Innate
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Lymphocyte Activation
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Mucocutaneous Lymph Node Syndrome / genetics
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Mucocutaneous Lymph Node Syndrome / immunology
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Mucocutaneous Lymph Node Syndrome / physiopathology
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Pandemics
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Pneumonia, Viral / genetics
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Pneumonia, Viral / immunology*
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Pneumonia, Viral / physiopathology
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Respiratory Insufficiency / genetics
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Respiratory Insufficiency / immunology*
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Respiratory Insufficiency / physiopathology
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SARS-CoV-2
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Severity of Illness Index