ArticleMicrobiology spectrum2025
Human PrP E219K: a new and promising substrate for robust RT-QuIC amplification of human prions with potential for strain discrimination.
Article in Microbiology spectrum, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Sporadic Creutzfeldt-Jakob disease: a multidimensional review from epidemiology to treatment and prognosis.Journal of neurology · 2026Review
- Advancing prion diagnostics: full-length human E200K RT-QuIC substrate facilitates prion detection in tear fluid and improves sensitivity in cerebrospinal fluid.Acta neuropathologica communications · 2026Article
- Identification and initial characterization of novel prion protein gene (Frontiers in veterinary science · 2026Article
- Recent advancements in QuIC-based diagnostic assays for sporadic and inherited prion diseases: focusing on the emerging role of ES-QuIC.Frontiers in neuroscience · 2026Review
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Authors and funding
9 authors.
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Abstract
Mammalian prion diseases are fatal neurodegenerative disorders caused by the conformational conversion of the host-encoded prion protein (PrP) into a pathogenic, misfolded isoform, known as PrP IMPORTANCE: Creutzfeldt-Jakob disease (CJD) is a fatal neurodegenerative disorder within the prion disease family. Definitive diagnosis and strain typing currently require post-mortem analyses. In this study, we demonstrate that the human PrP E219K variant serves as an effective substrate for prion in vitro amplification using real-time quaking-induced conversion. This substrate enables (i) rapid and robust amplification of the most common human prion strains and (ii) clear and direct discrimination between variant CJD and all tested sporadic CJD subtypes, based on statistical analyses of lag times of the prion amplification reactions. These findings represent a significant step toward the development of ante-mortem tools for prion strain typing in affected patients.
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