Evidence map›Paper›PMID 27344974›Full record

ArticleScientific reports2016

Highly pathogenic avian influenza H5N1 virus delays apoptotic responses via activation of STAT3.

Kenrie P Y Hui, Hung Sing Li, Man Chun Cheung, Renee W Y Chan, Kit M Yuen, Chris K P Mok, John M Nicholls, J S Malik Peiris, Michael C W Chan

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
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

9 authors at 2 institutions in 2 countries.

Kenrie P Y HuiCentre of Influenza Research and School of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Hung Sing LiCentre of Influenza Research and School of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Man Chun CheungCentre of Influenza Research and School of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Renee W Y ChanCentre of Influenza Research and School of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Kit M YuenCentre of Influenza Research and School of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Chris K P MokCentre of Influenza Research and School of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
John M NichollsDepartment of Pathology, LKS Faculty of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong SAR, China.
J S Malik PeirisCentre of Influenza Research and School of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Michael C W ChanCentre of Influenza Research and School of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
University of Hong Kong · HKChinese University of Hong Kong · CN

Funding

NIAID NIH HHS HHSN272201400006C
6 · The paper itself

Abstract

Highly pathogenic avian influenza (HPAI) H5N1 virus continues to pose pandemic threat, but there is a lack of understanding of its pathogenesis. We compared the apoptotic responses triggered by HPAI H5N1 and low pathogenic H1N1 viruses using physiologically relevant respiratory epithelial cells. We demonstrated that H5N1 viruses delayed apoptosis in primary human bronchial and alveolar epithelial cells (AECs) compared to H1N1 virus. Both caspase-8 and -9 were activated by H5N1 and H1N1 viruses in AECs, while H5N1 differentially up-regulated TRAIL. H5N1-induced apoptosis was reduced by TRAIL receptor silencing. More importantly, STAT3 knock-down increased apoptosis by H5N1 infection suggesting that H5N1 virus delays apoptosis through activation of STAT3. Taken together, we demonstrate that STAT3 is involved in H5N1-delayed apoptosis compared to H1N1. Since delay in apoptosis prolongs the duration of virus replication and production of pro-inflammatory cytokines and TRAIL from H5N1-infected cells, which contribute to orchestrate cytokine storm and tissue damage, our results suggest that STAT3 may play a previously unsuspected role in H5N1 pathogenesis.

Indexed as

AnimalsApoptosisBirdsBronchiCaspase 8Caspase 9Cell LineCells, CulturedCytokinesDogsEpithelial CellsHumansInflammationInfluenza A Virus, H1N1 SubtypeInfluenza A Virus, H5N1 SubtypeInfluenza, HumanCaspase 8Caspase 9CytokinesSTAT3 Transcription Factor

Identifiers

PMID27344974
PMCPMC4921847
OpenAlexW2465516807

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.