Abstract

Clinical outcome upon infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) ranges from silent infection to lethal coronavirus disease 2019 (COVID-19). We have found an enrichment in rare variants predicted to be loss-of-function (LOF) at the 13 human loci known to govern Toll-like receptor 3 (TLR3)- and interferon regulatory factor 7 (IRF7)-dependent type I interferon (IFN) immunity to influenza virus in 659 patients with life-threatening COVID-19 pneumonia relative to 534 subjects with asymptomatic or benign infection. By testing these and other rare variants at these 13 loci, we experimentally defined LOF variants underlying autosomal-recessive or autosomal-dominant deficiencies in 23 patients (3.5%) 17 to 77 years of age. We show that human fibroblasts with mutations affecting this circuit are vulnerable to SARS-CoV-2. Inborn errors of TLR3- and IRF7-dependent type I IFN immunity can underlie life-threatening COVID-19 pneumonia in patients with no prior severe infection.

Original languageEnglish
Article numbereabd4570
Pages (from-to)422-+
JournalScience
Volume370
Issue number6515
DOIs
Publication statusPublished - 23 Oct 2020

Keywords

  • Adolescent
  • Adult
  • Aged
  • Aged, 80 and over
  • Alleles
  • Asymptomatic Infections
  • Betacoronavirus
  • Child
  • Child, Preschool
  • Coronavirus Infections/genetics
  • Female
  • Genetic Loci
  • Genetic Predisposition to Disease
  • Humans
  • Infant
  • Interferon Regulatory Factor-7/deficiency
  • Interferon Type I/immunology
  • Loss of Function Mutation
  • Male
  • Middle Aged
  • Pandemics
  • Pneumonia, Viral/genetics
  • Receptor, Interferon alpha-beta/deficiency
  • Toll-Like Receptor 3/deficiency
  • Young Adult

Cite this