Evidence map›Paper›PMID 25033192›Full record

ArticlePloS one2014

Respiratory syncytial virus can infect basal cells and alter human airway epithelial differentiation.

B David Persson, Aron B Jaffe, Rachel Fearns, Henry Danahay

Abstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

66 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Frontiers in immunology · 2021
    Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Unique nasal cell states induced by common pediatric respiratory viruses.bioRxiv : the preprint server for biology · 2026
    Article
  8. RelA Signaling inInternational journal of molecular sciences · 2026
    Article
  9. bioRxiv : the preprint server for biology · 2026
    Article
  10. Article
  11. Risk factors for severe lower respiratory tract infection among children under 5 years of age hospitalized with respiratory syncytial virus.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025
    Observational
  12. CF airway epithelia display exaggerated host defense responses and prolonged cilia loss during RSV infection.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2025
    Article
  13. Article
  14. Article
  15. Article
  16. Introduction to Respiratory Syncytial Virus.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  17. Review
  18. Article
  19. Review
  20. Article

6 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

4 authors.

B David PerssonDevelopmental and Molecular Pathways, Novartis Institutes for BioMedical Research, Cambridge, Massachusetts, United States of America.
Aron B JaffeDevelopmental and Molecular Pathways, Novartis Institutes for BioMedical Research, Cambridge, Massachusetts, United States of America.
Rachel FearnsDepartment of Microbiology, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Henry DanahayRespiratory Disease Area, Novartis Institutes for BioMedical Research, Horsham, United Kingdom.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Respiratory syncytial virus (RSV) is a major cause of morbidity and mortality worldwide, causing severe respiratory illness in infants and immune compromised patients. The ciliated cells of the human airway epithelium have been considered to be the exclusive target of RSV, although recent data have suggested that basal cells, the progenitors for the conducting airway epithelium, may also become infected in vivo. Using either mechanical or chemical injury models, we have demonstrated a robust RSV infection of p63+ basal cells in air-liquid interface (ALI) cultures of human bronchial epithelial cells. In addition, proliferating basal cells in 2D culture were also susceptible to RSV infection. We therefore tested the hypothesis that RSV infection of this progenitor cell would influence the differentiation status of the airway epithelium. RSV infection of basal cells on the day of seeding (MOI≤0.0001), resulted in the formation of an epithelium that showed a profound loss of ciliated cells and gain of secretory cells as assessed by acetylated α-tubulin and MUC5AC/MUC5B immunostaining, respectively. The mechanism driving the switch in epithelial phenotype is in part driven by the induced type I and type III interferon response that we demonstrate is triggered early following RSV infection. Neutralization of this response attenuates the RSV-induced loss of ciliated cells. Together, these data show that through infection of proliferating airway basal cells, RSV has the potential to influence the cellular composition of the airway epithelium. The resulting phenotype might be expected to contribute towards both the severity of acute infection, as well as to the longer-term consequences of viral exacerbations in patients with pre-existing respiratory diseases.

Indexed as

Cell DifferentiationCell ProliferationCells, CulturedEpithelial CellsHumansInterferon LambdaInterferonsInterferon Type IInterleukinsMucin 5ACMucin-5BRespiratory MucosaRespiratory Syncytial VirusesRespiratory Syncytial Virus InfectionsStem CellsTubulinInterferon Lambdainterferon-lambda, humanInterferonsInterferon Type IInterleukinsMUC5AC protein, humanMUC5B protein, humanMucin 5ACMucin-5BTubulin

Identifiers

PMID25033192
PMCPMC4102526

What OpenQuestion holds

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Registered trials

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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.