ArticleProceedings of the National Academy of Sciences of the United States of America2003
Virus-like interference in the latency and prevention of Creutzfeldt-Jakob disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 36 citations in OpenAlex.
- Article
- Multiple aspects of amyloid dynamicsFrontiers in molecular neuroscience · 2024Article
- 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
- Environmental and host factors that contribute to prion strain evolution.Acta neuropathologica · 2021Review
- Nonpathogenic Heterologous Prions Can Interfere with Prion Infection in a Strain-Dependent Manner.Journal of virology · 2018Article
- Rapid chemical decontamination of infectious CJD and scrapie particles parallels treatments known to disrupt microbes and biofilms.Virulence · 2015Article
- Co-existence of distinct prion types enables conformational evolution of human PrPSc by competitive selection.The Journal of biological chemistry · 2013Article
- Prion strain interactions are highly selective.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Coinfecting prion strains compete for a limiting cellular resource.Journal of virology · 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
- Quantitative recovery of scrapie agent with minimal protein from highly infectious cultures.Viral immunology · 2008Article
- Two Creutzfeldt-Jakob disease agents reproduce prion protein-independent identities in cell cultures.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Scrapie protein degradation by cysteine proteases in CD11c+ dendritic cells and GT1-1 neuronal cells.Journal of virology · 2004Article
- Early induction of interferon-responsive mRNAs in Creutzfeldt-Jakob disease.Journal of neurovirology · 2004Article
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Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We previously showed that intracerebral (ic) inoculation of the attenuated SY strain of Creutzfeld-Jakob disease in mice could delay clinical signs and widespread neuropathology evoked by subsequent ic challenge with the more virulent FU strain. Using lower doses of SY and FU ic, we here demonstrate that mice can be protected well into old age without demonstrable neuropathology or pathologic prion protein (PrP-res). In contrast, parallel FU only controls became terminally diseased 1 year earlier. To determine whether factors elaborated in response to SY might be part of this effect, we evaluated brain and serum samples from additional parallel mice at 90 days after SY infection and just before FU challenge. The infectivity of FU preparations was significantly reduced by mixing with these fresh SY brain homogenates but not by mixing with SY serum samples, suggesting that brain cells were elaborating labile inhibitory factors that were part of the protective response. SY infectivity was too low to be detected in these brain homogenates. Although suppression could be overcome by higher FU doses ic, strong protection against maximal doses of FU was observed by using i.v. inoculations. Because myeloid microglia are infectious and also elaborate many factors in response to the foreign Creutzfeld-Jakob disease agent, it is likely that innate immunity underlies the profound protection shown here. In principle, it should be possible to artificially stimulate relevant myeloid pathways to better prevent and/or delay the clinical and pathological sequelae of these infections.
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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.