CJD and Scrapie Require Agent‐Associated Nucleic Acids for Infection

  title={CJD and Scrapie Require Agent‐Associated Nucleic Acids for Infection},
  author={Sotirios Botsios and Laura Manuelidis},
  journal={Journal of Cellular Biochemistry},
Unlike Alzheimer's and most other neurodegenerative diseases, Transmissible Spongiform Encephalopathies (TSEs) are all caused by actively replicating infectious particles of viral size and density. Different strain‐specific TSE agents cause CJD, kuru, scrapie and BSE, and all behave as latent viruses that evade adaptive immune responses and can persist for years in lymphoreticular tissues. A foreign viral structure with a nucleic acid genome best explains these TSE strains and their endemic and… 

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Prokaryotic SPHINX replication sequences are conserved in mammalian brain and participate in neurodegeneration

The evolutionary origin, spread, and neuropathology of SPHINX 1.8 REP sequences opens another unanticipated chapter for mammalian symbiotic interactions with environmental microbes.

Reduced Expression of Prion Protein With Increased Interferon-β Fail to Limit Creutzfeldt-Jakob Disease Agent Replication in Differentiating Neuronal Cells

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The “Jekyll and Hyde” Actions of Nucleic Acids on the Prion-like Aggregation of Proteins*

How nucleic acid binding might influence protein misfolding for both disease-related and benign, functional prions and why the line between bad and good amyloids might be more subtle than previously thought are discussed.

Prokaryotic SPHINX sequences are conserved in mammalian brain and participate in neurodegeneration

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To reexamine the intrinsic resistance of TSE agents to denaturation, a paradigm for less resistant viruses and microbes, a rapid and reproducible high yield agent isolation procedure from cultured cells that minimized PrP amyloid and other cellular proteins is developed.

Replication and spread of CJD, kuru and scrapie agents in vivo and in cell culture

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A streamlined, high‐yield purification of infectious FU‐CJD mouse brain particles with minimal PrP suggested that new therapies directed at retromer–vesicular trafficking in other neurodegenerative diseases may also counteract late‐onset sCJD PrP amyloid pathology.

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The development of tissue culture models that support the replication of many different strains of agent and can produce high levels of infectivity are developed, providing new ways to rapidly identify intrinsic viral and strain‐specific molecules so important for diagnosis, prevention, and fundamental understanding.

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