ArticleJournal of virology2003
Subclinical prion disease induced by oral inoculation.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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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Who cites it
17 citing papers in PubMed, 41 citations in OpenAlex.
- No evidence of subclinical infection in sheep surviving oral challenge with prions.The Journal of general virology · 2025Article
- Subclinical infection occurs frequently following low dose exposure to prions by blood transfusion.Scientific reports · 2022Article
- Oral Ingestion of Synthetically Generated Recombinant Prion Is Sufficient to Cause Prion Disease in Wild-Type Mice.Pathogens (Basel, Switzerland) · 2020Article
- Review
- Prions: generation and spread versus neurotoxicity.The Journal of biological chemistry · 2014Review
- Prion neuropathology follows the accumulation of alternate prion protein isoforms after infective titre has peaked.Nature communications · 2014Article
- Disease characteristics of bovine spongiform encephalopathy following inoculation into mice via three different routes.International journal of experimental pathology · 2013Article
- Article
- Evaluation of the possible transmission of BSE and scrapie to gilthead sea bream (Sparus aurata).PloS one · 2009Article
- Prion strain discrimination based on rapid in vivo amplification and analysis by the cell panel assay.PloS one · 2009Article
- Molecular and transmission characteristics of primary-passaged ovine scrapie isolates in conventional and ovine PrP transgenic mice.Journal of virology · 2008Article
- The prion strain phenomenon: molecular basis and unprecedented features.Biochimica et biophysica acta · 2007Review
- Characterization of the genomic region containing the Shadow of Prion Protein (SPRN) gene in sheep.BMC genomics · 2007Article
- Extraneural prion neuroinvasion without lymphoreticular system infection.Journal of virology · 2005Article
- Protease-resistant human prion protein and ferritin are cotransported across Caco-2 epithelial cells: implications for species barrier in prion uptake from the intestine.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Accelerated prion disease in the absence of interleukin-10.Journal of virology · 2004Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Natural transmission of prion disease is believed to occur by peripheral infection such as oral inoculation. Following this route of inoculation, both the peripheral nervous system and the lymphoreticular system may be involved in the subsequent neuroinvasion of the central nervous system by prions, which may not necessarily result in clinical signs of terminal disease. Subclinical prion disease, characterized by the presence of infectivity and PrP(Sc) in the absence of overt clinical signs, may occur. It is not known which host factors contribute to whether infection with prions culminates in a terminal or subclinical disease state. We have investigated whether the level of host PrP(c) protein expression is a factor in the development of subclinical prion disease. When RML prion inoculum was inoculated by either the i.c. or intraperitoneal route, wild-type and tga20 mice both succumbed to terminal prion disease. In contrast, orally inoculated tga20 mice succumbed to terminal prion disease, whereas wild-type mice showed no clinical signs. However, wild-type mice sacrificed 375 or 525 days after oral inoculation harbored significant levels of brain PrP(Sc) and infectivity. These data show that same-species transmission of prions by the oral route in animals that express normal levels of PrP(c) can result in subclinical prion disease. This indicates that the level of host PrP(c) protein expression is a contributing factor to the regulation of development of terminal prion disease. Events that increase PrP(c) expression may predispose a prion-infected animal to the more deleterious effects of prion pathology.
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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.