Evidence map›Paper›PMID 23100363›Full record

ArticleThe Journal of general virology2013

Mucosal transmission and pathogenesis of chronic wasting disease in ferrets.

Matthew R Perrott, Christina J Sigurdson, Gary L Mason, Edward A Hoover

Abstract read
In one paragraph

Article in The Journal of general virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Review
  3. The ecology of chronic wasting disease in wildlife.Biological reviews of the Cambridge Philosophical Society · 2020
    Review
  4. Article
  5. Review
  6. Article
  7. Article
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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

4 authors at 3 institutions in 2 countries.

Matthew R PerrottPathobiology, Institute of Veterinary, Animal and Biomedical Sciences, Massey University, Palmerston North, New Zealand.
Christina J SigurdsonDepartment of Pathology, School of Medicine University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Gary L MasonPrion Research Center, Department of Microbiology, Immunology and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins CO 80523, USA.
Edward A HooverPrion Research Center, Department of Microbiology, Immunology and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins CO 80523, USA.
Colorado State University · USMassey University · NZUniversity of California, San Diego · US

Funding

Mechanisms of Prion Aggregation and Species BarriersR01NS069566 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ESKO, JEFFREY D, RAVITS, JOHN · 2011 to 2025
$5.7M
Transmission and Pathogenesis of Chronic Wasting Disease (CWD)R01NS061902 · NINDS · COLORADO STATE UNIVERSITY · PI MATHIASON, CANDACE K. · 2009 to 2022
$5.3M
Mechanisms of Prion SpreadR01NS076896 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SIGURDSON, CHRISTINA · 2012 to 2021
$3.4M
U.S. BASED COLLABORATION IN EMERGING VIRAL AND PRION DISEASES-N01AI025491 · NIAID · COLORADO STATE UNIVERSITY-FORT COLLINS · 2003 to 2003
–
NIAID NIH HHS N01 AI025491NINDS NIH HHS R01 NS061902NINDS NIH HHS R01-NS-061902NINDS NIH HHS R01 NS069566NINDS NIH HHS R01 NS076896
6 · The paper itself

Abstract

Chronic wasting disease (CWD) of cervids is almost certainly transmitted by mucosal contact with the causative prion, whether by direct (animal-to-animal) or indirect (environmental) means. Yet the sites and mechanisms of prion entry remain to be further understood. This study sought to extend this understanding by demonstrating that ferrets exposed to CWD via several mucosal routes developed infection, CWD prion protein (PrP(CWD)) amplification in lymphoid tissues, neural invasion and florid transmissible spongiform encephalopathy lesions resembling those in native cervid hosts. The ferrets developed extensive PrP(CWD) accumulation in the nervous system, retina and olfactory epithelium, with lesser deposition in tongue, muscle, salivary gland and the vomeronasal organ. PrP(CWD) accumulation in mucosal sites, including upper respiratory tract epithelium, olfactory epithelium and intestinal Peyer's patches, make the shedding of prions by infected ferrets plausible. It was also observed that regionally targeted exposure of the nasopharyngeal mucosa resulted in an increased attack rate when compared with oral exposure. The latter finding suggests that nasal exposure enhances permissiveness to CWD infection. The ferret model has further potential for investigation of portals for initiation of CWD infection.

Indexed as

Disease Models, AnimalDisease Transmission, InfectiousFerretsAnimalsAnimal StructuresMucous MembranePrionsWasting Disease, ChronicPrions

Identifiers

PMID23100363
PMCPMC3709615
OpenAlexW1991730805

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.