Evidence map›Paper›PMID 32587093›Full record

ArticleThe Journal of biological chemistry2020

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

Ulrike Felgenhauer, Andreas Schoen, Hans Henrik Gad, Rune Hartmann, Andreas R Schaubmar, Klaus Failing, Christian Drosten, Friedemann Weber

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 167 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
167citing papers in PubMed, 1 pooled it
5.8field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

167 citing papers in PubMed, 1 synthesis or guideline pooled it, 269 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Interferon Lambda: The Next Frontier in Antiviral Therapy?Pharmaceuticals (Basel, Switzerland) · 2025
    Review
  7. Article
  8. Heat-killedFrontiers in cellular and infection microbiology · 2025
    Article
  9. IFN Lambda Deficiency Contributes to Severe COVID-19 Outcomes.International journal of molecular sciences · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

107 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Ulrike FelgenhauerInstitute for Virology, FB10-Veterinary Medicine, Justus Liebig University, Giessen, Germany.ORCID 0000-0002-9478-5368
Andreas SchoenInstitute for Virology, FB10-Veterinary Medicine, Justus Liebig University, Giessen, Germany.
Hans Henrik GadDepartment for Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark.
Rune HartmannDepartment for Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark.
Andreas R SchaubmarUnit for Biomathematics and Data Processing, FB10-Veterinary Medicine, Justus Liebig University, Giessen, Germany.
Klaus FailingUnit for Biomathematics and Data Processing, FB10-Veterinary Medicine, Justus Liebig University, Giessen, Germany.
Christian DrostenGerman Centre for Infection Research (DZIF), partner sites Giessen and Charité Berlin, Germany.
Friedemann WeberInstitute for Virology, FB10-Veterinary Medicine, Justus Liebig University, Giessen, Germany friedemann.weber@vetmed.uni-giessen.de.ORCID 0000-0001-9737-337X
Justus-Liebig-Universität Gießen · DEAarhus University · DKHumboldt-Universität zu Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

AnimalsAntiviral AgentsBetacoronavirusCell LineChlorocebus aethiopsCoronavirus InfectionsCOVID-19HumansInterferon LambdaInterferonsInterferon Type IJanus KinasesNitrilesPandemicsPneumonia, ViralPyrazolesAntiviral AgentsInterferon LambdaInterferonsInterferon Type IJanus KinasesNitrilesPyrazolesPyrimidinesruxolitinibantiviral agentCOVID-19cytokine actioninfectioninnate immunityinterferoninterferon-alpha/betainterferon-lambdaruxolitinibSARS–CoV-2virologyvirus

Identifiers

PMID32587093
PMCPMC7549028
OpenAlexW3037578804

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.