Evidence map›Paper›PMID 27357918›Full record

ArticleScientific reports2016

A clinically authentic mouse model of enterovirus 71 (EV-A71)-induced neurogenic pulmonary oedema.

Carla Bianca Luena Victorio, Yishi Xu, Qimei Ng, Beng Hooi Chua, Sylvie Alonso, Vincent T K Chow, Kaw Bing Chua

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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Validation of Lung [Molecular imaging and biology · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Observational
  10. Article
  11. Mast cells contribute to Enterovirus 71 infection-induced pulmonary edema in neonatal mice.Laboratory investigation; a journal of technical methods and pathology · 2018
    Article
  12. The association between acute flaccid myelitis (AFM) and Enterovirus D68 (EV-D68) - what is the evidence for causation?Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin · 2018
    Review
  13. 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

7 authors at 3 institutions in 2 countries.

Carla Bianca Luena VictorioTemasek Lifesciences Laboratory, 1 Research Link, National University of Singapore, Singapore.
Yishi XuTemasek Lifesciences Laboratory, 1 Research Link, National University of Singapore, Singapore.
Qimei NgTemasek Lifesciences Laboratory, 1 Research Link, National University of Singapore, Singapore.
Beng Hooi ChuaOffice of Research and Development, Curtin University, Perth, Western Australia, Australia.
Sylvie AlonsoDepartment of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Vincent T K ChowDepartment of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Kaw Bing ChuaTemasek Lifesciences Laboratory, 1 Research Link, National University of Singapore, Singapore.
National University of Singapore · SGTemasek Life Sciences Laboratory · SGCurtin University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enterovirus 71 (EV-A71) is a neurotropic virus that sporadically causes fatal neurologic illness among infected children. Animal models of EV-A71 infection exist, but they do not recapitulate in animals the spectrum of disease and pathology observed in fatal human cases. Specifically, neurogenic pulmonary oedema (NPE)-the main cause of EV-A71 infection-related mortality-is not observed in any of these models. This limits their utility in understanding viral pathogenesis of neurologic infections. We report the development of a mouse model of EV-A71 infection displaying NPE in severely affected animals. We inoculated one-week-old BALB/c mice with an adapted EV-A71 strain and identified clinical signs consistent with observations in human cases and other animal models. We also observed respiratory distress in some mice. At necropsy, we found their lungs to be heavier and incompletely collapsed compared to other mice. Serum levels of catecholamines and histopathology of lung and brain tissues of these mice strongly indicated onset of NPE. The localization of virally-induced brain lesions also suggested a potential pathogenic mechanism for EV-A71-induced NPE. This novel mouse model of virally-induced NPE represents a valuable resource for studying viral mechanisms of neuro-pathogenesis and pre-clinical testing of potential therapeutics and prophylactics against EV-A71-related neurologic complications.

Indexed as

AnimalsAntibodies, NeutralizingBrainCatecholaminesDisease Models, AnimalEnterovirus A, HumanEnterovirus InfectionsHumansKaplan-Meier EstimateLungMiceMice, Inbred BALB CPulmonary EdemaSeverity of Illness IndexAntibodies, NeutralizingCatecholamines

Identifiers

PMID27357918
PMCPMC4928123
OpenAlexW2466575300

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.