Inhibition of SARS-CoV-2 by type I and type III interferons

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

DOI

  • Ulrike Felgenhauer, Justus Liebig University Giessen, Giessen, Germany.
  • ,
  • Andreas Schoen, Justus Liebig University Giessen, Giessen, Germany.
  • ,
  • Hans Henrik Gad
  • Rune Hartmann
  • Andreas R Schaubmar, Justus Liebig University Giessen, Giessen, Germany.
  • ,
  • Klaus Failing, Justus Liebig University Giessen, Giessen, Germany.
  • ,
  • Christian Drosten, German Centre for Infection Research (DZIF), partner sites Giessen and Charité Berlin, Humboldt-Universität zu Berlin
  • ,
  • Friedemann Weber, Justus Liebig University Giessen, Giessen, Germany., German Centre for Infection Research (DZIF), partner sites Giessen and Charité Berlin

The recently emerged severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the causative agent of the devastating COVID-19 lung disease pandemic. Here, we tested the inhibitory activities of the antiviral interferons of type I (IFN-α) and type III (IFN-λ) against SARS-CoV-2 and compared them with those against SARS-CoV-1, which emerged in 2003. Using two mammalian epithelial cell lines (human Calu-3 and simian Vero E6), we found that both IFNs dose-dependently inhibit SARS-CoV-2. In contrast, SARS-CoV-1 was restricted only by IFN-α in these cell lines. SARS-CoV-2 generally exhibited a broader IFN sensitivity than SARS-CoV-1. Moreover, ruxolitinib, an inhibitor of IFN-triggered Janus kinase/signal transducer and activator of transcription signaling, boosted SARS-CoV-2 replication in the IFN-competent Calu-3 cells. We conclude that SARS-CoV-2 is sensitive to exogenously added IFNs. This finding suggests that type I and especially the less adverse effect-prone type III IFN are good candidates for the management of COVID-19.

OriginalsprogEngelsk
TidsskriftThe Journal of Biological Chemistry
Vol/bind295
Nummer41
Antal sider7
ISSN0021-9258
DOI
StatusUdgivet - okt. 2020

Bibliografisk note

Published under license by The American Society for Biochemistry and Molecular Biology, Inc.

Se relationer på Aarhus Universitet Citationsformater

ID: 192362550