Interleukin-1 in COVID-19 Infection: Immunopathogenesis and Possible Therapeutic Perspective

Viral Immunol. 2021 Dec;34(10):679-688. doi: 10.1089/vim.2021.0071. Epub 2021 Dec 8.

Abstract

The newfound coronavirus disease 2019 (COVID-19), initiated by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is an international public health concern, threatening the lives of millions of people worldwide. The virus seems to have a propensity to infect older males, especially those with underlying diseases. The cytokine storm following hyperactivated immune responses due to SARS-CoV-2 infection is probably the crucial source of severe pneumonia that leads to acute lung injury, systemic inflammatory response syndrome, or acute respiratory distress syndrome, and finally multiple organ dysfunction syndromes, as well as death in many cases. Several studies revealed that interleukin (IL)-1β levels were elevated during COVID-19 infection. In addition, the IL-1 cytokine family has a pivotal role in the induction of cytokine storm due to uncontrolled immune responses in COVID-19 infection. This article reviews the role of IL-1 in inflammation and utilization of IL-1 inhibitor agents in controlling the inflammatory outcomes initiated by SARS-CoV-2 infection.

Keywords: COVID-19; IL-1; SARS-CoV-2; cytokine inhibitors.

Publication types

  • Review

MeSH terms

  • Acute Lung Injury / drug therapy
  • Acute Lung Injury / immunology
  • Acute Lung Injury / pathology
  • COVID-19 / immunology*
  • COVID-19 / mortality
  • COVID-19 / pathology
  • COVID-19 Drug Treatment*
  • Cytokine Release Syndrome / drug therapy*
  • Cytokine Release Syndrome / immunology
  • Cytokine Release Syndrome / pathology
  • Humans
  • Interleukin-1 / antagonists & inhibitors
  • Interleukin-1 / immunology*
  • Multiple Organ Failure / drug therapy
  • Multiple Organ Failure / immunology
  • Multiple Organ Failure / pathology
  • Respiratory Distress Syndrome / drug therapy
  • Respiratory Distress Syndrome / immunology
  • Respiratory Distress Syndrome / pathology
  • SARS-CoV-2 / immunology
  • SARS-CoV-2 / pathogenicity

Substances

  • Interleukin-1