Evidence map›Paper›PMID 26809688›Full record

ArticleVirulence2016

Induction of DNA double-strand breaks and cellular senescence by human respiratory syncytial virus.

Isidoro Martínez, Verónica García-Carpizo, Trinidad Guijarro, Ana García-Gomez, Diego Navarro, Ana Aranda, Alberto Zambrano

Open access · goldAbstract read
In one paragraph

Article in Virulence, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

47 citing papers in PubMed, 63 citations in OpenAlex.

  1. Trial
  2. Article
  3. Viruses · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. [Mechanism and significance of cell senescence induced by viral infection].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. COVID-19 and cellular senescence.Nature reviews. Immunology · 2023
    Review
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Isidoro Martíneza Department of Molecular Pathology , Spanish National Center for Microbiology, Institute of Health Carlos III , Madrid , Spain.
Verónica García-Carpizob Department of Endocrine Physiopathology and Nervous System , Institute for Biomedical Research (IIBM), CSIC-UAM , Madrid , Spain.
Trinidad Guijarroa Department of Molecular Pathology , Spanish National Center for Microbiology, Institute of Health Carlos III , Madrid , Spain.
Ana García-Gomeza Department of Molecular Pathology , Spanish National Center for Microbiology, Institute of Health Carlos III , Madrid , Spain.
Diego Navarrob Department of Endocrine Physiopathology and Nervous System , Institute for Biomedical Research (IIBM), CSIC-UAM , Madrid , Spain.
Ana Arandab Department of Endocrine Physiopathology and Nervous System , Institute for Biomedical Research (IIBM), CSIC-UAM , Madrid , Spain.
Alberto Zambranoa Department of Molecular Pathology , Spanish National Center for Microbiology, Institute of Health Carlos III , Madrid , Spain.
Instituto de Salud Carlos III · ESUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human respiratory syncytial virus (HRSV) accounts for the majority of lower respiratory tract infections during infancy and childhood and is associated with significant morbidity and mortality. HRSV provokes a proliferation arrest and characteristic syncytia in cellular systems such as immortalized epithelial cells. We show here that HRSV induces the expression of DNA damage markers and proliferation arrest such as P-TP53, P-ATM, CDKN1A and γH2AFX in cultured cells secondary to the production of mitochondrial reactive oxygen species (ROS). The DNA damage foci contained γH2AFX and TP53BP1, indicative of double-strand breaks (DSBs) and could be reversed by antioxidant treatments such as N-Acetylcysteine (NAC) or reduced glutathione ethyl ester (GSHee). The damage observed is associated with the accumulation of senescent cells, displaying a canonical senescent phenotype in both mononuclear cells and syncytia. In addition, we show signs of DNA damage and aging such as γH2AFX and CDKN2A expression in the respiratory epithelia of infected mice long after viral clearance. Altogether, these results show that HRSV triggers a DNA damage-mediated cellular senescence program probably mediated by oxidative stress. The results also suggest that this program might contribute to the physiopathology of the infection, tissue remodeling and aging, and might be associated to long-term consequences of HRSV infections.

Indexed as

Cellular SenescenceDNA Breaks, Double-StrandedHost-Pathogen InteractionsA549 CellsAcetylcysteineAnimalsCell LineCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p18DNA DamageGlutathioneHistonesHumansMiceOxidative StressReactive Oxygen SpeciesAcetylcysteineCDKN2A protein, humanCdkn2a protein, mouseCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p18gamma-H2AX protein, mouseGlutathioneH2AX protein, humanHistonesReactive Oxygen SpeciesS-ethyl glutathionecellular senescenceDNA damagehuman respiratoryROSsyncytial virus

Identifiers

PMID26809688
PMCPMC4871660
OpenAlexW2311703219

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.