ArticleJournal of virology2010
Coinfecting prion strains compete for a limiting cellular resource.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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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.
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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.
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Who cites it
66 citing papers in PubMed, 85 citations in OpenAlex.
- The axonal transport velocity of prions is independent of prion formation.PLoS pathogens · 2026Article
- Co-infection with two α-synuclein strains reveals novel synergistic interactions.Acta neuropathologica · 2025Article
- Co-infection with two α-synuclein strains reveals novel synergistic interactions.bioRxiv : the preprint server for biology · 2025Article
- Evidence of a novel α-synuclein strain isolated from a Parkinson's disease with dementia patient sample.Acta neuropathologica communications · 2025Article
- The Evolution of Experimental Rodent Models for Prion Diseases.Journal of neurochemistry · 2025Review
- Article
- Effect of host and strain factors on α-synuclein prion pathogenesis.Trends in neurosciences · 2024Review
- Multiple aspects of amyloid dynamicsFrontiers in molecular neuroscience · 2024Article
- Evidence for preexisting prion substrain diversity in a biologically cloned prion strain.PLoS pathogens · 2023Article
- Article
- The G51D SNCA mutation generates a slowly progressive α-synuclein strain in early-onset Parkinson's disease.Acta neuropathologica communications · 2023Article
- Prion strains: shining new light on old concepts.Cell and tissue research · 2023Review
- Development of a methodology for large-scale production of prions for biological and structural studies.Frontiers in molecular biosciences · 2023Article
- North American and Norwegian Chronic Wasting Disease Prions Exhibit Different Potential for Interspecies Transmission and Zoonotic Risk.The Journal of infectious diseases · 2022Article
- Efficient interspecies transmission of synthetic prions.PLoS pathogens · 2021Article
- Environmental and host factors that contribute to prion strain evolution.Acta neuropathologica · 2021Review
- BSE can propagate in sheep co-infected or pre-infected with scrapie.Scientific reports · 2021Article
- Host prion protein expression levels impact prion tropism for the spleen.PLoS pathogens · 2020Article
- The role of prion strain diversity in the development of successful therapeutic treatments.Progress in molecular biology and translational science · 2020Review
- Alteration of Prion Strain Emergence by Nonhost Factors.mSphere · 2019Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Prion strain interference can influence the emergence of a dominant strain from a mixture; however, the mechanisms underlying prion strain interference are poorly understood. In our model of strain interference, inoculation of the sciatic nerve with the drowsy (DY) strain of the transmissible mink encephalopathy (TME) agent prior to superinfection with the hyper (HY) strain of TME can completely block HY TME from causing disease. We show here that the deposition of PrP(Sc), in the absence of neuronal loss or spongiform change, in the central nervous system corresponds with the ability of DY TME to block HY TME infection. This suggests that DY TME agent-induced damage is not responsible for strain interference but rather prions compete for a cellular resource. We show that protein misfolding cyclic amplification (PMCA) of DY and HY TME maintains the strain-specific properties of PrP(Sc) and replicates infectious agent and that DY TME can interfere, or completely block, the emergence of HY TME. DY PrP(Sc) does not convert all of the available PrP(C) to PrP(Sc) in PMCA, suggesting the mechanism of prion strain interference is due to the sequestering of PrP(C) and/or other cellular components required for prion conversion. The emergence of HY TME in PMCA was controlled by the initial ratio of the TME agents. A higher ratio of DY to HY TME agent is required for complete blockage of HY TME in PMCA compared to several previous in vivo studies, suggesting that HY TME persists in animals coinfected with the two strains. This was confirmed by PMCA detection of HY PrP(Sc) in animals where DY TME had completely blocked HY TME from causing disease.
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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.