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


Journal

The Journal of biological chemistry
ISSN: 1083-351X
Titre abrégé: J Biol Chem
Pays: United States
ID NLM: 2985121R

Informations de publication

Date de publication:
09 10 2020
Historique:
received: 07 04 2020
revised: 24 06 2020
pubmed: 27 6 2020
medline: 22 10 2020
entrez: 27 6 2020
Statut: ppublish

Résumé

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.

Identifiants

pubmed: 32587093
pii: S0021-9258(17)49795-X
doi: 10.1074/jbc.AC120.013788
pmc: PMC7549028
doi:

Substances chimiques

Antiviral Agents 0
Interferon Type I 0
Nitriles 0
Pyrazoles 0
Pyrimidines 0
ruxolitinib 82S8X8XX8H
Interferons 9008-11-1
Janus Kinases EC 2.7.10.2
Interferon Lambda 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

13958-13964

Informations de copyright

© 2020 Felgenhauer et al.

Déclaration de conflit d'intérêts

Conflict of interest—The authors declare that they have no conflicts of interest with the contents of this article.

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Auteurs

Ulrike Felgenhauer (U)

Institute for Virology, FB10-Veterinary Medicine, Justus Liebig University, Giessen, Germany.

Andreas Schoen (A)

Institute for Virology, FB10-Veterinary Medicine, Justus Liebig University, Giessen, Germany.

Hans Henrik Gad (HH)

Department for Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark.

Rune Hartmann (R)

Department for Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark.

Andreas R Schaubmar (AR)

Unit for Biomathematics and Data Processing, FB10-Veterinary Medicine, Justus Liebig University, Giessen, Germany.

Klaus Failing (K)

Unit for Biomathematics and Data Processing, FB10-Veterinary Medicine, Justus Liebig University, Giessen, Germany.

Christian Drosten (C)

German Centre for Infection Research (DZIF), partner sites Giessen and Charité Berlin, Germany.
Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute of Virology, Berlin, Germany.

Friedemann Weber (F)

Institute for Virology, FB10-Veterinary Medicine, Justus Liebig University, Giessen, Germany friedemann.weber@vetmed.uni-giessen.de.
German Centre for Infection Research (DZIF), partner sites Giessen and Charité Berlin, Germany.

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