ArticleJournal of cellular biochemistry2009
Strain-specific viral properties of variant Creutzfeldt-Jakob disease (vCJD) are encoded by the agent and not by host prion protein.
Article in Journal of cellular biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 33 citations in OpenAlex.
- Decellularized small intestine scaffolds: a potential xenograft for restoration of intestinal perforation.Tissue barriers · 2024Article
- Development of decellularization protocol for caprine small intestine submucosa as a biomaterial.Biomaterials and biosystems · 2022Article
- Decellularization of caprine esophagus using fruit pericarp extract of Sapindus mukorossi.Cell and tissue banking · 2022Article
- Reduced Expression of Prion Protein With Increased Interferon-β Fail to Limit Creutzfeldt-Jakob Disease Agent Replication in Differentiating Neuronal Cells.Frontiers in physiology · 2022Article
- Proteomic analysis of host brain components that bind to infectious particles in Creutzfeldt-Jakob disease.Proteomics · 2015Article
- Susceptibility of GT1-7 cells to mouse-passaged field scrapie isolates with a long incubation.Prion · 2014Article
- Review
- Acinetobacter phage genome is similar to Sphinx 2.36, the circular DNA copurified with TSE infected particles.Scientific reports · 2013Article
- Mouse-adapted scrapie strains 139A and ME7 overcome species barrier to induce experimental scrapie in hamsters and changed their pathogenic features.Virology journal · 2012Article
- Continuous production of prions after infectious particles are eliminated: implications for Alzheimer's disease.PloS one · 2012Article
- Candidate cell substrates, vaccine production, and transmissible spongiform encephalopathies.Emerging infectious diseases · 2011Article
- High CJD infectivity remains after prion protein is destroyed.Journal of cellular biochemistry · 2011Article
- Fukuoka-1 strain of transmissible spongiform encephalopathy agent infects murine bone marrow-derived cells with features of mesenchymal stem cells.Transfusion · 2011Article
- Nuclease resistant circular DNAs copurify with infectivity in scrapie and CJD.Journal of neurovirology · 2011Article
- Proliferative arrest of neural cells induces prion protein synthesis, nanotube formation, and cell-to-cell contacts.Journal of cellular biochemistry · 2010Article
- Agent-specific Shadoo responses in transmissible encephalopathies.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2010Article
- The kuru infectious agent is a unique geographic isolate distinct from Creutzfeldt-Jakob disease and scrapie agents.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Human CJD, endemic sheep scrapie, epidemic bovine spongiform encephalopathy (BSE), and other transmissible spongiform encephalopathies (TSEs), are caused by a group of related but molecularly uncharacterized infectious agents. The UK-BSE agent infected many species, including humans where it causes variant CJD (vCJD). As in most viral infections, different TSE disease phenotypes are determined by both the agent strain and the host species. TSE strains are most reliably classified by incubation time and regional neuropathology in mice expressing wild-type (wt) prion protein (PrP). We compared vCJD to other human and animal derived TSE strains in both mice and neuronal cultures expressing wt murine PrP. Primary and serial passages of the human vCJD agent, as well as the highly selected mutant 263K sheep scrapie agent, revealed profound strain-specific characteristics were encoded by the agent, not by host PrP. Prion theory posits that PrP converts itself into the infectious agent, and thus short incubations require identical PrP sequences in the donor and recipient host. However, wt PrP mice injected with human vCJD brain homogenates showed dramatically shorter primary incubation times than mice expressing only human PrP, a finding not in accord with a PrP species barrier. All mouse passage brains showed the vCJD agent derived from a stable BSE strain. Additionally, both vCJD brain and monotypic neuronal cultures produced a diagnostic 19 kDa PrP fragment previously observed only in BSE and vCJD primate brains. Monotypic cultures can be used to identify the intrinsic, strain-determining molecules of TSE infectious particles.
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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.