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Infection of Primary Nasal Epithelial Cells Grown at an Air-Liquid Interface to Characterize Human Coronavirus-Host Interactions
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Type 2 and interferon inflammation regulate SARS-CoV-2 entry factor expression in the airway epithelium

Satria P Sajuthi1, Peter DeFord1, Yingchun Li1

  • 1Center for Genes, Environment, and Health, National Jewish Health, Denver, CO, USA.

Nature Communications
|October 13, 2020
PubMed

Insights

Genetics influence ACE2 and TMPRSS2 expression in airways, impacting SARS-CoV-2 entry. Viral infections and inflammation, particularly interleukin-13, modulate these host factors, affecting COVID-19 outcomes.

Area of Science:

  • Genetics
  • Immunology
  • Virology

Background:

  • Severe Acute Respiratory Syndrome-Coronavirus 2 (SARS-CoV-2) uses host ACE2 and TMPRSS2 proteins for cell entry.
  • Understanding the regulation of these entry factors is crucial for comprehending SARS-CoV-2 tropism and COVID-19 pathogenesis.

Purpose of the Study:

  • To investigate the role of genetics and co-expression networks in regulating ACE2 and TMPRSS2 expression in the pediatric airway.
  • To elucidate the impact of inflammation and viral infections on these host factors.

Main Methods:

  • Analysis of nasal airway transcriptome data from 695 children.
  • Identification of expression quantitative trait loci (eQTLs) for ACE2 and TMPRSS2.
  • Examination of co-expression networks and the influence of inflammatory mediators like interleukin-13 (IL-13) and interferon response.

Main Results:

  • Expression quantitative trait loci for ACE2 and TMPRSS2 were identified, with varying population frequencies.
  • TMPRSS2 was found to be part of a mucus secretory network upregulated by type 2 (T2) inflammation via IL-13.
  • Interferon response to viruses significantly upregulated ACE2 expression, an effect also observed at the protein level.
  • Common coronavirus infections in children induced host responses including IL6 and ACE2 upregulation.

Conclusions:

  • Genetic variations influence ACE2 and TMPRSS2 expression levels in the airway.
  • Interleukin-13-driven T2 inflammation and viral interferon responses play significant roles in regulating SARS-CoV-2 entry factors.
  • These findings provide insights into mechanisms affecting SARS-CoV-2 infectivity and COVID-19 clinical outcomes.

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