Evidence map›Paper›PMID 32903043›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2020

Human coronaviruses 229E and OC43 replicate and induce distinct antiviral responses in differentiated primary human bronchial epithelial cells.

Su-Ling Loo, Peter A B Wark, Camille Esneau, Kristy S Nichol, Alan C-Y Hsu, Nathan W Bartlett

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 14% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Frontiers in immunology · 2021
    Pooled it
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  9. Human coronaviruses: activation and antagonism of innate immune responses.Microbiology and molecular biology reviews : MMBR · 2025
    Review
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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

6 authors at 2 institutions in 1 country.

Su-Ling LooViral Immunology and Respiratory Disease group, University of Newcastle, Newcastle, New South Wales, Australia.
Peter A B WarkPriority Research Centre for Healthy Lungs, University of Newcastle and Hunter Medical Research Institute, Newcastle, New South Wales, Australia.ORCID 0000-0001-5676-6126
Camille EsneauViral Immunology and Respiratory Disease group, University of Newcastle, Newcastle, New South Wales, Australia.ORCID 0000-0002-5479-1851
Kristy S NicholPriority Research Centre for Healthy Lungs, University of Newcastle and Hunter Medical Research Institute, Newcastle, New South Wales, Australia.
Alan C-Y HsuPriority Research Centre for Healthy Lungs, University of Newcastle and Hunter Medical Research Institute, Newcastle, New South Wales, Australia.
Nathan W BartlettViral Immunology and Respiratory Disease group, University of Newcastle, Newcastle, New South Wales, Australia.ORCID 0000-0002-2715-5163
Hunter Medical Research Institute · AUJohn Hunter Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The recurrent emergence of novel, pathogenic coronaviruses (CoVs) severe acute respiratory syndrome coronavirus 1 (SARS-CoV-1; 2002), Middle East respiratory syndrome (MERS)-CoV (2012), and most recently SARS-CoV-2 (2019) has highlighted the need for physiologically informative airway epithelial cell infection models for studying immunity to CoVs and development of antiviral therapies. To address this, we developed an in vitro infection model for two human coronaviruses; alphacoronavirus 229E-CoV (229E) and betacoronavirus OC43-CoV (OC43) in differentiated primary human bronchial epithelial cells (pBECs). Primary BECs from healthy subjects were grown at air-liquid interface (ALI) and infected with 229E or OC43, and replication kinetics and time-course expression of innate immune mediators were assessed. OC43 and 229E-CoVs replicated in differentiated pBECs but displayed distinct replication kinetics: 229E replicated rapidly with viral load peaking at 24 h postinfection, while OC43 replication was slower peaking at 96 h after infection. This was associated with diverse antiviral response profiles defined by increased expression of type I/III interferons and interferon-stimulated genes (ISGs) by 229E compared with no innate immune activation with OC43 infection. Understanding the host-virus interaction for previously established coronaviruses will give insight into pathogenic mechanisms underpinning SARS-CoV-2-induced respiratory disease and other future coronaviruses that may arise from zoonotic sources.

Indexed as

Antiviral AgentsBronchiCells, CulturedCoronavirus 229E, HumanCoronavirus InfectionsEpithelial CellsHumansInterferon LambdaInterferonsVirus ReplicationAntiviral AgentsInterferon LambdaInterferons229Ecoronavirusepithelial cellinfectionOC43

Identifiers

PMID32903043
PMCPMC7758816
OpenAlexW3084001932

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.