SARS-CoV-2 evades immune detection in alveolar macrophages

EMBO Rep. 2020 Dec 3;21(12):e51252. doi: 10.15252/embr.202051252. Epub 2020 Oct 28.

Abstract

Respiratory infections, like the current COVID-19 pandemic, target epithelial cells in the respiratory tract. Alveolar macrophages (AMs) are tissue-resident macrophages located within the lung. They play a key role in the early phases of an immune response to respiratory viruses. AMs are likely the first immune cells to encounter SARS-CoV-2 during an infection, and their reaction to the virus will have a profound impact on the outcome of the infection. Interferons (IFNs) are antiviral cytokines and among the first cytokines produced upon viral infection. In this study, AMs from non-infectious donors are challenged with SARS-CoV-2. We demonstrate that challenged AMs are incapable of sensing SARS-CoV-2 and of producing an IFN response in contrast to other respiratory viruses, like influenza A virus and Sendai virus, which trigger a robust IFN response. The absence of IFN production in AMs upon challenge with SARS-CoV-2 could explain the initial asymptotic phase observed during COVID-19 and argues against AMs being the sources of pro-inflammatory cytokines later during infection.

Keywords: COVID-19; SARS-CoV-2; alveolar macrophages; interferon; interferon lambda.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antiviral Agents / immunology
  • COVID-19 / immunology*
  • COVID-19 / virology
  • Cells, Cultured
  • Cytokines / immunology
  • Epithelial Cells / immunology
  • Epithelial Cells / virology
  • Humans
  • Immune Evasion
  • Interferon Type I / immunology
  • Lung / immunology
  • Lung / virology
  • Macrophages, Alveolar / immunology*
  • Macrophages, Alveolar / virology*
  • Pandemics
  • SARS-CoV-2 / immunology*

Substances

  • Antiviral Agents
  • Cytokines
  • Interferon Type I