An Impaired Inflammatory and Innate Immune Response in COVID-19

Mol Cells. 2021 Jun 30;44(6):384-391. doi: 10.14348/molcells.2021.0068.

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.

Publication types

  • Review

MeSH terms

  • Anti-Inflammatory Agents / therapeutic use
  • COVID-19 / immunology*
  • COVID-19 / mortality
  • COVID-19 / virology
  • COVID-19 Drug Treatment
  • Cytokine Release Syndrome / drug therapy
  • Cytokine Release Syndrome / immunology*
  • Cytokine Release Syndrome / mortality
  • Cytokine Release Syndrome / virology
  • Dexamethasone / therapeutic use
  • Gene Expression Regulation
  • Host-Pathogen Interactions / genetics
  • Host-Pathogen Interactions / immunology*
  • Humans
  • Immunity, Innate / drug effects
  • Inflammation
  • Interferon Type I / genetics
  • Interferon Type I / immunology
  • Interleukins / genetics
  • Interleukins / immunology
  • SARS-CoV-2 / immunology
  • SARS-CoV-2 / pathogenicity*
  • Severe Acute Respiratory Syndrome / drug therapy
  • Severe Acute Respiratory Syndrome / immunology*
  • Severe Acute Respiratory Syndrome / mortality
  • Severe Acute Respiratory Syndrome / virology
  • Severity of Illness Index
  • Signal Transduction
  • Survival Analysis

Substances

  • Anti-Inflammatory Agents
  • Interferon Type I
  • Interleukins
  • Dexamethasone