COVID-19: immunopathogenesis and Immunotherapeutics

Signal Transduct Target Ther. 2020 Jul 25;5(1):128. doi: 10.1038/s41392-020-00243-2.

Abstract

The recent novel coronavirus disease (COVID-19) outbreak, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is seeing a rapid increase in infected patients worldwide. The host immune response to SARS-CoV-2 appears to play a critical role in disease pathogenesis and clinical manifestations. SARS-CoV-2 not only activates antiviral immune responses, but can also cause uncontrolled inflammatory responses characterized by marked pro-inflammatory cytokine release in patients with severe COVID-19, leading to lymphopenia, lymphocyte dysfunction, and granulocyte and monocyte abnormalities. These SARS-CoV-2-induced immune abnormalities may lead to infections by microorganisms, septic shock, and severe multiple organ dysfunction. Therefore, mechanisms underlying immune abnormalities in patients with COVID-19 must be elucidated to guide clinical management of the disease. Moreover, rational management of the immune responses to SARS-CoV-2, which includes enhancing anti-viral immunity while inhibiting systemic inflammation, may be key to successful treatment. In this review, we discuss the immunopathology of COVID-19, its potential mechanisms, and clinical implications to aid the development of new therapeutic strategies against COVID-19.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Betacoronavirus* / immunology
  • Betacoronavirus* / pathogenicity
  • COVID-19
  • Coronavirus Infections* / epidemiology
  • Coronavirus Infections* / immunology
  • Coronavirus Infections* / therapy
  • Cytokines / immunology
  • Disease Outbreaks*
  • Humans
  • Immunity, Innate*
  • Immunotherapy*
  • Pandemics*
  • Pneumonia, Viral* / epidemiology
  • Pneumonia, Viral* / immunology
  • Pneumonia, Viral* / therapy
  • SARS-CoV-2
  • Shock, Septic* / epidemiology
  • Shock, Septic* / immunology
  • Shock, Septic* / therapy

Substances

  • Cytokines