Evidence map›Paper›PMID 25100723›Full record

ArticleThe Journal of biological chemistry2014

Genotype-dependent molecular evolution of sheep bovine spongiform encephalopathy (BSE) prions in vitro affects their zoonotic potential.

Zuzana Krejciova, Marcelo A Barria, Michael Jones, James W Ironside, Martin Jeffrey, Lorenzo González, Mark W Head

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Prion diseases: Lessons from historical outbreaks and potential emerging ones.Protein science : a publication of the Protein Society · 2025
    Review
  2. Article
  3. Generation of human chronic wasting disease in transgenic mice.Acta neuropathologica communications · 2021
    Article
  4. Review
  5. Article
  6. Human stem cell-derived astrocytes replicate human prions in aThe Journal of experimental medicine · 2017
    Article
  7. 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 1 country.

Zuzana KrejciovaNational Creutzfeldt-Jakob Disease Research and Surveillance Unit, The University of Edinburgh, Edinburgh EH4 2XU, United Kingdom.
Marcelo A BarriaNational Creutzfeldt-Jakob Disease Research and Surveillance Unit, The University of Edinburgh, Edinburgh EH4 2XU, United Kingdom.
Michael JonesScottish National Blood Transfusion Service, Edinburgh EH17 7QT, United Kingdom, and.
James W IronsideNational Creutzfeldt-Jakob Disease Research and Surveillance Unit, The University of Edinburgh, Edinburgh EH4 2XU, United Kingdom.
Martin JeffreyAnimal Health and Veterinary Laboratories Agency, Lasswade, Edinburgh EH26 0PZ, United Kingdom.
Lorenzo GonzálezAnimal Health and Veterinary Laboratories Agency, Lasswade, Edinburgh EH26 0PZ, United Kingdom.
Mark W HeadNational Creutzfeldt-Jakob Disease Research and Surveillance Unit, The University of Edinburgh, Edinburgh EH4 2XU, United Kingdom,. Electronic address: m.w.head@ed.ac.uk.
University of Edinburgh · GBAnimal and Plant Health Agency · GBScottish National Blood Transfusion Service · GB

Funding

Department of HealthMedical Research Council G0600953Medical Research Council G0900580
6 · The paper itself

Abstract

Prion diseases are rare fatal neurological conditions of humans and animals, one of which (variant Creutzfeldt-Jakob disease) is known to be a zoonotic form of the cattle disease bovine spongiform encephalopathy (BSE). What makes one animal prion disease zoonotic and others not is poorly understood, but it appears to involve compatibility between the prion strain and the host prion protein sequence. Concerns have been raised that the United Kingdom sheep flock may have been exposed to BSE early in the cattle BSE epidemic and that serial BSE transmission in sheep might have resulted in adaptation of the agent, which may have come to phenotypically resemble scrapie while maintaining its pathogenicity for humans. We have modeled this scenario in vitro. Extrapolation from our results suggests that if BSE were to infect sheep in the field it may, with time and in some sheep genotypes, become scrapie-like at the molecular level. However, the results also suggest that if BSE in sheep were to come to resemble scrapie it would lose its ability to affect humans.

Indexed as

AnimalsBrainCattleEncephalopathy, Bovine SpongiformEvolution, MolecularGenotypeGlycosylationHumansPrionsProtein FoldingProtein Processing, Post-TranslationalScrapieSheep, DomesticZoonosesPrionsMolecular EvolutionPrionPrion DiseaseProtein ConformationProtein MisfoldingProtein Misfolding Cyclic AmplificationSheep BSEZoonosis

Identifiers

PMID25100723
PMCPMC4176218
OpenAlexW2045722044

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.