ArticleJournal of virology2006
Strain fidelity of chronic wasting disease upon murine adaptation.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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.
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.
Who cites it
43 citing papers in PubMed, 77 citations in OpenAlex.
- Neuronal Ndst1 depletion accelerates prion protein clearance and slows neurodegeneration in prion infection.PLoS pathogens · 2023Article
- Chronic wasting disease in Europe: new strains on the horizon.Acta veterinaria Scandinavica · 2021Review
- Review
- Cervid Prion Protein Polymorphisms: Role in Chronic Wasting Disease Pathogenesis.International journal of molecular sciences · 2021Review
- Prion protein post-translational modifications modulate heparan sulfate binding and limit aggregate size in prion disease.Neurobiology of disease · 2020Article
- Prion protein glycans reduce intracerebral fibril formation and spongiosis in prion disease.The Journal of clinical investigation · 2020Article
- Shortening heparan sulfate chains prolongs survival and reduces parenchymal plaques in prion disease caused by mobile, ADAM10-cleaved prions.Acta neuropathologica · 2020Article
- Generation of novel neuroinvasive prions following intravenous challenge.Brain pathology (Zurich, Switzerland) · 2018Article
- Molecular Mechanisms of Chronic Wasting Disease Prion Propagation.Cold Spring Harbor perspectives in medicine · 2018Review
- Scientific opinion on chronic wasting disease (II).EFSA journal. European Food Safety Authority · 2018Article
- Prion Strains and Transmission Barrier Phenomena.Pathogens (Basel, Switzerland) · 2018Review
- Article
- Enhanced neuroinvasion by smaller, soluble prions.Acta neuropathologica communications · 2017Article
- Post-translational modifications in PrP expand the conformational diversity of prions in vivo.Scientific reports · 2017Article
- Chronic wasting disease (CWD) in cervids.EFSA journal. European Food Safety Authority · 2017Article
- Insights into Mechanisms of Transmission and Pathogenesis from Transgenic Mouse Models of Prion Diseases.Methods in molecular biology (Clifton, N.J.) · 2017Review
- Cross-species transmission of CWD prions.Prion · 2016Review
- Unique Properties of the Rabbit Prion Protein Oligomer.PloS one · 2016Article
- Transgenic Mouse Bioassay: Evidence That Rabbits Are Susceptible to a Variety of Prion Isolates.PLoS pathogens · 2015Article
- Human prion protein sequence elements impede cross-species chronic wasting disease transmission.The Journal of clinical investigation · 2015Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
Chronic wasting disease (CWD), a prion disease of deer and elk, is highly prevalent in some regions of North America. The establishment of mouse-adapted CWD prions has proven difficult due to the strong species barrier between mice and deer. Here we report the efficient transmission of CWD to transgenic mice overexpressing murine PrP. All mice developed disease 500 +/- 62 days after intracerebral CWD challenge. The incubation period decreased to 228 +/- 103 days on secondary passage and to 162 +/- 6 days on tertiary passage. Mice developed very large, radially structured cerebral amyloid plaques similar to those of CWD-infected deer and elk. PrP(Sc) was detected in spleen, indicating that murine CWD was lymphotropic. PrP(Sc) glycoform profiles maintained a predominantly diglycosylated PrP pattern, as seen with CWD in deer and elk, across all passages. Therefore, all pathological, biochemical, and histological strain characteristics of CWD appear to persist upon repetitive serial passage through mice. These findings indicate that the salient strain-specific properties of CWD are encoded by agent-intrinsic components rather than by host factors.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.