ArticlePLoS pathogens2014
Evidence that bank vole PrP is a universal acceptor for prions.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 113 citations in OpenAlex.
- From a prion seed to a tree of discoveries: Byron Caughey's RT-QuIC legacy in protein misfolding research.Acta neuropathologica · 2026Review
- Leveraging the dominant-negative effect of the kuru-protective G127V prion protein variant as a novel therapeutic strategy.Neurobiology of disease · 2026Article
- A self-complementary recombinant adeno-associated virus vector coding for an anchorless prion protein carrying the G127V mutation extends survival in a rodent prion disease model.PLoS pathogens · 2026Article
- A Neuronal Cell Line Model for Studying Camel Prions.Pathogens (Basel, Switzerland) · 2026Article
- A self-complementary recombinant adeno-associated virus vector coding for an anchorless prion protein carrying the G127V mutation extends survival in a rodent prion disease model.bioRxiv : the preprint server for biology · 2026Article
- Leveraging the dominant-negative effect of the kuru-protective G127V prion protein variant as a novel therapeutic strategy.bioRxiv : the preprint server for biology · 2026Article
- Overexpression of bank vole PrP(I109) in mice induces a spontaneous atypical prion disease with sex-dependent onset, early NfL elevation, and universal prion strain permissiveness.Acta neuropathologica communications · 2026Article
- Recent advancements in QuIC-based diagnostic assays for sporadic and inherited prion diseases: focusing on the emerging role of ES-QuIC.Frontiers in neuroscience · 2026Review
- Substitution of histidine 95 by tyrosine in the prion protein causes spontaneous neurodegeneration in transgenic mice.PLoS pathogens · 2025Article
- Different folding mechanisms in prion proteins from mammals with different disease susceptibility observed at the single-molecule level.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Transmission and Characterization of Creutzfeldt-Jakob Disease and Chronic Wasting Disease in the North American Deer Mouse.Viruses · 2025Article
- Overview of North American Isolates of Chronic Wasting Disease Used for Strain Research.Pathogens (Basel, Switzerland) · 2025Review
- Cofactors facilitate bona fide prion misfolding in vitro but are not necessary for the infectivity of recombinant murine prions.PLoS pathogens · 2025Article
- Prion Disease Diagnostic Biomarker Utility in Pre-symptomatic Disease.Sub-cellular biochemistry · 2025Review
- The molecular determinants of a universal prion acceptor.PLoS pathogens · 2024Article
- Convergent generation of atypical prions in knockin mouse models of genetic prion disease.The Journal of clinical investigation · 2024Article
- A Protein Misfolding Shaking Amplification-based method for the spontaneous generation of hundreds of bona fide prions.Nature communications · 2024Article
- Cell biology of prion strains in vivo and in vitro.Cell and tissue research · 2023Review
- New developments in prion disease research using genetically modified mouse models.Cell and tissue research · 2023Review
- A single protective polymorphism in the prion protein blocks cross-species prion replication in cultured cells.Journal of neurochemistry · 2023Article
23 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Bank voles are uniquely susceptible to a wide range of prion strains isolated from many different species. To determine if this enhanced susceptibility to interspecies prion transmission is encoded within the sequence of the bank vole prion protein (BVPrP), we inoculated Tg(M109) and Tg(I109) mice, which express BVPrP containing either methionine or isoleucine at polymorphic codon 109, with 16 prion isolates from 8 different species: humans, cattle, elk, sheep, guinea pigs, hamsters, mice, and meadow voles. Efficient disease transmission was observed in both Tg(M109) and Tg(I109) mice. For instance, inoculation of the most common human prion strain, sporadic Creutzfeldt-Jakob disease (sCJD) subtype MM1, into Tg(M109) mice gave incubation periods of ∼200 days that were shortened slightly on second passage. Chronic wasting disease prions exhibited an incubation time of ∼250 days, which shortened to ∼150 days upon second passage in Tg(M109) mice. Unexpectedly, bovine spongiform encephalopathy and variant CJD prions caused rapid neurological dysfunction in Tg(M109) mice upon second passage, with incubation periods of 64 and 40 days, respectively. Despite the rapid incubation periods, other strain-specified properties of many prion isolates--including the size of proteinase K-resistant PrPSc, the pattern of cerebral PrPSc deposition, and the conformational stability--were remarkably conserved upon serial passage in Tg(M109) mice. Our results demonstrate that expression of BVPrP is sufficient to engender enhanced susceptibility to a diverse range of prion isolates, suggesting that BVPrP may be a universal acceptor for prions.
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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.