ArticleJournal of virology2005
Extraneural prion neuroinvasion without lymphoreticular system infection.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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.
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.
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Who cites it
46 citing papers in PubMed, 81 citations in OpenAlex.
- Bovine Spongiform Encephalopathy: An Integrated Review of Prion Mechanisms, Neuroanatomy, and Control.Veterinary sciences · 2026Review
- 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
- The Evolution of Experimental Rodent Models for Prion Diseases.Journal of neurochemistry · 2025Review
- A-synuclein prion strains differentially adapt after passage in mice.PLoS pathogens · 2024Article
- Review
- Evidence for preexisting prion substrain diversity in a biologically cloned prion strain.PLoS pathogens · 2023Article
- Article
- Vaccines for prion diseases: a realistic goal?Cell and tissue research · 2023Review
- Prion strains associated with iatrogenic CJD in French and UK human growth hormone recipients.Acta neuropathologica communications · 2021Article
- Environmental and host factors that contribute to prion strain evolution.Acta neuropathologica · 2021Review
- Cervid Prion Protein Polymorphisms: Role in Chronic Wasting Disease Pathogenesis.International journal of molecular sciences · 2021Review
- Detection of Pathognomonic Biomarker PrPBiomolecules · 2020Review
- Prion strain-dependent tropism is maintained between spleen and granuloma and relies on lymphofollicular structures.Scientific reports · 2019Article
- Alteration of Prion Strain Emergence by Nonhost Factors.mSphere · 2019Article
- Prion protein polymorphisms associated with reduced CWD susceptibility limit peripheral PrPBMC veterinary research · 2019Article
- Complement Regulatory Protein Factor H Is a Soluble Prion Receptor That Potentiates Peripheral Prion Pathogenesis.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Enhanced neuroinvasion by smaller, soluble prions.Acta neuropathologica communications · 2017Article
- PrPSc formation and clearance as determinants of prion tropism.PLoS pathogens · 2017Article
- Role of Prion Replication in the Strain-dependent Brain Regional Distribution of Prions.The Journal of biological chemistry · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
While prion infection of the lymphoreticular system (LRS) is necessary for neuroinvasion in many prion diseases, in bovine spongiform encephalopathy and atypical cases of sheep scrapie there is evidence to challenge that LRS infection is required for neuroinvasion. Here we investigated the role of prion infection of LRS tissues in neuroinvasion following extraneural inoculation with the HY and DY strains of the transmissible mink encephalopathy (TME) agent. DY TME agent infectivity was not detected in spleen or lymph nodes following intraperitoneal inoculation and clinical disease was not observed following inoculation into the peritoneum or lymph nodes, or after oral ingestion. In contrast, inoculation of the HY TME agent by each of these peripheral routes resulted in replication in the spleen and lymph nodes and induced clinical disease. To clarify the role of the LRS in neuroinvasion, the HY and DY TME agents were also inoculated into the tongue because it is densely innervated and lesions on the tongue, which are common in ruminants, increase the susceptibility of hamsters to experimental prion disease. Following intratongue inoculation, the DY TME agent caused prion disease and was detected in both the tongue and brainstem nuclei that innervate the tongue, but the prion protein PrP(Sc) was not detected in the spleen or lymph nodes. These findings indicate that the DY TME agent can spread from the tongue to the brain along cranial nerves and neuroinvasion does not require agent replication in the LRS. These studies provide support for prion neuroinvasion from highly innervated peripheral tissues in the absence of LRS infection in natural prion diseases of livestock.
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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.