Evidence map›Paper›PMID 37197656›Full record

ArticleFrontiers in immunology2023

Interferon regulatory factor 3 mediates effective antiviral responses to human coronavirus 229E and OC43 infection.

Joseph K Sampson Duncan, Danyang Xu, Maria Licursi, Michael A Joyce, Holly A Saffran, Kaiwen Liu, Jin Gohda, D Lorne Tyrrell, Yasushi Kawaguchi, Kensuke Hirasawa

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Genetic and chemical correction of cystic fibrosis reduces airway susceptibility to SARS-CoV-2.American journal of physiology. Lung cellular and molecular physiology · 2026
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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

10 authors at 3 institutions in 2 countries.

Joseph K Sampson DuncanDivision of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, NL, Canada.
Danyang XuDivision of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, NL, Canada.
Maria LicursiDivision of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, NL, Canada.
Michael A JoyceLi Ka Shing Institute of Virology, University of Alberta, Edmonton, AB, Canada.
Holly A SaffranLi Ka Shing Institute of Virology, University of Alberta, Edmonton, AB, Canada.
Kaiwen LiuDivision of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, NL, Canada.
Jin GohdaResearch Center for Asian Infectious Diseases, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
D Lorne TyrrellLi Ka Shing Institute of Virology, University of Alberta, Edmonton, AB, Canada.
Yasushi KawaguchiResearch Center for Asian Infectious Diseases, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Kensuke HirasawaDivision of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, NL, Canada.
Memorial University of Newfoundland · CAUniversity of Alberta · CAThe University of Tokyo · JP

Funding

CIHR PJT-153238CIHR VR-3172645
6 · The paper itself

Abstract

Interferon regulatory factors (IRFs) are key elements of antiviral innate responses that regulate the transcription of interferons (IFNs) and IFN-stimulated genes (ISGs). While the sensitivity of human coronaviruses to IFNs has been characterized, antiviral roles of IRFs during human coronavirus infection are not fully understood. Type I or II IFN treatment protected MRC5 cells from human coronavirus 229E infection, but not OC43. Cells infected with 229E or OC43 upregulated ISGs, indicating that antiviral transcription is not suppressed. Antiviral IRFs, IRF1, IRF3 and IRF7, were activated in cells infected with 229E, OC43 or severe acute respiratory syndrome-associated coronavirus 2 (SARS-CoV-2). RNAi knockdown and overexpression of IRFs demonstrated that IRF1 and IRF3 have antiviral properties against OC43, while IRF3 and IRF7 are effective in restricting 229E infection. IRF3 activation effectively promotes transcription of antiviral genes during OC43 or 229E infection. Our study suggests that IRFs may be effective antiviral regulators against human coronavirus infection.

Indexed as

Coronavirus 229E, HumanCOVID-19Antiviral AgentsHumansInterferon Regulatory Factor-3Interferon Regulatory FactorsInterferonsSARS-CoV-2Antiviral AgentsInterferon Regulatory Factor-3Interferon Regulatory FactorsInterferons229Einnate immunityinterferonIRF1IRF3IRF7OC43SARS-CoV2

Identifiers

PMID37197656
PMCPMC10183588
OpenAlexW4367625901

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.