Evidence map›Paper›PMID 31299975›Full record

ArticleRespiratory research2019

Rhinovirus replication and innate immunity in highly differentiated human airway epithelial cells.

Stephanie M Warner, Shahina Wiehler, Aubrey N Michi, David Proud

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Vaccines for the common cold.The Cochrane database of systematic reviews · 2022
    Pooled it
  2. Trial
  3. Lower viral loads in subjects with rhinovirus-challenged allergy despite reduced innate immunity.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2022
    Trial
  4. Article
  5. Article
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  7. Article
  8. Review
  9. Review
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  11. Quantifying Rhinovirus Genomic and Negative-Strand RNA by RT-PCR.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  12. A novelThe European respiratory journal · 2024
    Article
  13. Article
  14. Review
  15. Article
  16. Article
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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

4 authors at 1 institution in 1 country.

Stephanie M WarnerDepartment of Physiology & Pharmacology and Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, 3280 Hospital Drive NW, Calgary, AB, T2N 4Z6, Canada.
Shahina WiehlerDepartment of Physiology & Pharmacology and Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, 3280 Hospital Drive NW, Calgary, AB, T2N 4Z6, Canada.
Aubrey N MichiDepartment of Physiology & Pharmacology and Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, 3280 Hospital Drive NW, Calgary, AB, T2N 4Z6, Canada.
David ProudDepartment of Physiology & Pharmacology and Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, 3280 Hospital Drive NW, Calgary, AB, T2N 4Z6, Canada. dproud@ucalgary.ca.ORCID http://orcid.org/0000-0001-9629-6595
University of Calgary · CA

Funding

Natural Science and Engineering Research Council of Canada RGPIN-2018-03861
6 · The paper itself

Abstract

backgroundHuman rhinovirus (HRV) infections are the primary cause of the common cold and are a major trigger for exacerbations of lower airway diseases, such as asthma and chronic obstructive pulmonary diseases. Although human bronchial epithelial cells (HBE) are the natural host for HRV infections, much of our understanding of how HRV replicates and induces host antiviral responses is based on studies using non-airway cell lines (e.g. HeLa cells). The current study examines the replication cycle of HRV, and host cell responses, in highly differentiated cultures of HBE.

methodsHighly differentiated cultures of HBE were exposed to initial infectious doses ranging from 10

resultsRegardless of initial infectious dose, relatively constant levels of both genomic and negative strand RNA are generated during replication, with negative strand copy numbers being10,000-fold lower than those of genomic strands. Infections were limited to a small percentage of ciliated cells and did not result in any overt signs of epithelial death. Importantly, regardless of infectious dose, HRV-16 infections were cleared by HBE in the absence of immune cells. Levels of type I and type III interferons (IFNs) varied with initial infectious dose, implying that factors other than levels of double-stranded RNA regulate IFN induction, but the time-course of HRV-16 clearance HBE was the same regardless of levels of IFNs produced. Patterns of antiviral viperin and ISG15 expression suggest they may be generated in an IFN-independent manner during HRV-16 infections.

conclusionsThese data challenge a number of aspects of dogma generated from studies in HeLa cells and emphasize the importance of appropriate cell context when studying HRV infections.

Indexed as

Cell DifferentiationCells, CulturedHumansImmunity, InnateRespiratory MucosaRhinovirusVirus ReplicationHighly differentiated human airway epithelial cellsHuman rhinovirusInterferonsNegative strand templateViperinViral clearance

Identifiers

PMID31299975
PMCPMC6626354
OpenAlexW2956951246

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.