ArticleProceedings of the National Academy of Sciences of the United States of America2009
The kuru infectious agent is a unique geographic isolate distinct from Creutzfeldt-Jakob disease and scrapie agents.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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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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
27 citing papers in PubMed, 42 citations in OpenAlex.
- Article
- Infecting human brain organoids with FFI or sCJD preserves prion traits regardless of host genotype.NPJ dementia · 2025Article
- Review
- Infections and immunity: associations with obesity and related metabolic disorders.Journal of pathology and translational medicine · 2023Review
- 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
- Prion protein PrP nucleic acid binding and mobilization implicates retroelements as the replicative component of transmissible spongiform encephalopathy.Archives of virology · 2020Review
- Kuru, the First Human Prion Disease.Viruses · 2019Review
- A prokaryotic viral sequence is expressed and conserved in mammalian brain.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Viral Infections and Obesity.Current obesity reports · 2017Review
- Proteomic analysis of host brain components that bind to infectious particles in Creutzfeldt-Jakob disease.Proteomics · 2015Article
- Rapid chemical decontamination of infectious CJD and scrapie particles parallels treatments known to disrupt microbes and biofilms.Virulence · 2015Article
- Pawnobiome: manipulation of the hologenome within one host generation and beyond.Frontiers in microbiology · 2015Article
- Highly infectious CJD particles lack prion protein but contain many viral-linked peptides by LC-MS/MS.Journal of cellular biochemistry · 2014Article
- Susceptibility of GT1-7 cells to mouse-passaged field scrapie isolates with a long incubation.Prion · 2014Article
- Kuru: a journey back in time from papua new Guinea to the neanderthals' extinction.Pathogens (Basel, Switzerland) · 2013Review
- Review
- Acinetobacter phage genome is similar to Sphinx 2.36, the circular DNA copurified with TSE infected particles.Scientific reports · 2013Article
- Continuous production of prions after infectious particles are eliminated: implications for Alzheimer's disease.PloS one · 2012Article
- An overview of human prion diseases.Virology journal · 2011Review
- High CJD infectivity remains after prion protein is destroyed.Journal of cellular biochemistry · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Human sporadic Creutzfeldt-Jakob disease (sCJD), endemic sheep scrapie, and epidemic bovine spongiform encephalopathy (BSE) are caused by a related group of infectious agents. The new U.K. BSE agent spread to many species, including humans, and clarifying the origin, specificity, virulence, and diversity of these agents is critical, particularly because infected humans do not develop disease for many years. As with viruses, transmissible spongiform encephalopathy (TSE) agents can adapt to new species and become more virulent yet maintain fundamentally unique and stable identities. To make agent differences manifest, one must keep the host genotype constant. Many TSE agents have revealed their independent identities in normal mice. We transmitted primate kuru, a TSE once epidemic in New Guinea, to mice expressing normal and approximately 8-fold higher levels of murine prion protein (PrP). High levels of murine PrP did not prevent infection but instead shortened incubation time, as would be expected for a viral receptor. Sporadic CJD and BSE agents and representative scrapie agents were clearly different from kuru in incubation time, brain neuropathology, and lymphoreticular involvement. Many TSE agents can infect monotypic cultured GT1 cells, and unlike sporadic CJD isolates, kuru rapidly and stably infected these cells. The geographic independence of the kuru agent provides additional reasons to explore causal environmental pathogens in these infectious neurodegenerative diseases.
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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.