Evidence map›Paper›PMID 23236380›Full record

ArticlePloS one2012

Genetic predictions of prion disease susceptibility in carnivore species based on variability of the prion gene coding region.

Paula Stewart, Lauren Campbell, Susan Skogtvedt, Karen A Griffin, Jon M Arnemo, Morten Tryland, Simon Girling, Michael W Miller, Michael A Tranulis, Wilfred Goldmann

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

31 citing papers in PubMed, 45 citations in OpenAlex.

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  8. Article
  9. Review
  10. Article
  11. Novel Polymorphisms and Genetic Characteristics of the Prion Protein Gene (International journal of molecular sciences · 2020
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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

10 authors at 7 institutions in 4 countries.

Paula StewartNeurobiology Division, The Roslin Institute & R(D)SVS, University of Edinburgh, Roslin, United Kingdom.
Lauren Campbell
Susan Skogtvedt
Karen A Griffin
Jon M Arnemo
Morten Tryland
Simon Girling
Michael W Miller
Michael A Tranulis
Wilfred Goldmann
Colorado Parks and Wildlife · USNorwegian University of Life Sciences · NOUniversity of Edinburgh · GBGenØk · NORoslin Institute · GBRoyal Zoological Society of Scotland · GBSwedish University of Agricultural Sciences · SE

Funding

Biotechnology and Biological Sciences Research Council BBS/E/A/00001652Biotechnology and Biological Sciences Research Council BBS/E/D/05241340Biotechnology and Biological Sciences Research Council BBS/E/D/20251967Biotechnology and Biological Sciences Research Council BBS/E/D/20251968
6 · The paper itself

Abstract

Mammalian species vary widely in their apparent susceptibility to prion diseases. For example, several felid species developed prion disease (feline spongiform encephalopathy or FSE) during the bovine spongiform encephalopathy (BSE) epidemic in the United Kingdom, whereas no canine BSE cases were detected. Whether either of these or other groups of carnivore species can contract other prion diseases (e.g. chronic wasting disease or CWD) remains an open question. Variation in the host-encoded prion protein (PrP(C)) largely explains observed disease susceptibility patterns within ruminant species, and may explain interspecies differences in susceptibility as well. We sequenced and compared the open reading frame of the PRNP gene encoding PrP(C) protein from 609 animal samples comprising 29 species from 22 genera of the Order Carnivora; amongst these samples were 15 FSE cases. Our analysis revealed that FSE cases did not encode an identifiable disease-associated PrP polymorphism. However, all canid PrPs contained aspartic acid or glutamic acid at codon 163 which we propose provides a genetic basis for observed susceptibility differences between canids and felids. Among other carnivores studied, wolverine (Gulo gulo) and pine marten (Martes martes) were the only non-canid species to also express PrP-Asp163, which may impact on their prion diseases susceptibility. Populations of black bear (Ursus americanus) and mountain lion (Puma concolor) from Colorado showed little genetic variation in the PrP protein and no variants likely to be highly resistant to prions in general, suggesting that strain differences between BSE and CWD prions also may contribute to the limited apparent host range of the latter.

Indexed as

Genetic Predisposition to DiseaseAllelesAnimalsCarnivoraGene FrequencyGenotypePolymorphism, GeneticPolymorphism, Single NucleotidePrion DiseasesPrionsSpecies SpecificityPrions

Identifiers

PMID23236380
PMCPMC3517517
OpenAlexW2141169243

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.