Leveraging the antiviral type I interferon system as a first line of defense against SARS-CoV-2 pathogenicity

Immunity. 2021 Mar 9;54(3):557-570.e5. doi: 10.1016/j.immuni.2021.01.017. Epub 2021 Jan 29.

Abstract

The emergence and spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has resulted in significant global morbidity, mortality, and societal disruption. A better understanding of virus-host interactions may potentiate therapeutic insights toward limiting this infection. Here we investigated the dynamics of the systemic response to SARS-CoV-2 in hamsters by histological analysis and transcriptional profiling. Infection resulted in consistently high levels of virus in the upper and lower respiratory tracts and sporadic occurrence in other distal tissues. A longitudinal cohort revealed a wave of inflammation, including a type I interferon (IFN-I) response, that was evident in all tissues regardless of viral presence but was insufficient to prevent disease progression. Bolstering the antiviral response with intranasal administration of recombinant IFN-I reduced viral disease, prevented transmission, and lowered inflammation in vivo. This study defines the systemic host response to SARS-CoV-2 infection and supports use of intranasal IFN-I as an effective means of early treatment.

Keywords: COVID-19; IFN-I; cytokine; hamster; intranasal; mRNA-seq; pandemic; prophylactic; therapeutic; transcriptomics.

Publication types

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

MeSH terms

  • Animals
  • Biopsy
  • COVID-19 / genetics
  • COVID-19 / immunology
  • COVID-19 / metabolism*
  • COVID-19 / virology*
  • Cricetinae
  • Cytokines / genetics
  • Cytokines / metabolism
  • Disease Models, Animal
  • Gene Expression Profiling
  • Host-Pathogen Interactions* / immunology
  • Humans
  • Immunity, Innate
  • Interferon Type I / genetics
  • Interferon Type I / metabolism*
  • Lung / immunology
  • Lung / metabolism
  • Lung / pathology
  • Lung / virology
  • Organ Specificity / immunology
  • SARS-CoV-2 / physiology*
  • Virulence
  • Virus Replication / immunology

Substances

  • Cytokines
  • Interferon Type I