Abstract
The recent appearance of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has affected millions of people around the world and caused a global pandemic of coronavirus disease 2019 (COVID-19). It has been suggested that uncontrolled, exaggerated inflammation contributes to the adverse outcomes of COVID-19. In this review, we summarize our current understanding of the innate immune response elicited by SARS-CoV-2 infection and the hyperinflammation that contributes to disease severity and death. We also discuss the immunological determinants behind COVID-19 severity and propose a rationale for the underlying mechanisms.
Keywords:
COVID-19; cytokine storm; immunoparalysis; inflammatory cytokines; innate immune response.
MeSH terms
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Anti-Inflammatory Agents / therapeutic use
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COVID-19 / immunology*
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COVID-19 / mortality
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COVID-19 / virology
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COVID-19 Drug Treatment
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Cytokine Release Syndrome / drug therapy
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Cytokine Release Syndrome / immunology*
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Cytokine Release Syndrome / mortality
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Cytokine Release Syndrome / virology
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Dexamethasone / therapeutic use
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Gene Expression Regulation
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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 / drug effects
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Inflammation
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Interferon Type I / genetics
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Interferon Type I / immunology
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Interleukins / genetics
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Interleukins / immunology
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SARS-CoV-2 / immunology
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SARS-CoV-2 / pathogenicity*
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Severe Acute Respiratory Syndrome / drug therapy
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Severe Acute Respiratory Syndrome / immunology*
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Severe Acute Respiratory Syndrome / mortality
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Severe Acute Respiratory Syndrome / virology
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Severity of Illness Index
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Signal Transduction
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Survival Analysis
Substances
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Anti-Inflammatory Agents
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Interferon Type I
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Interleukins
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Dexamethasone