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Related Experiment Videos

CJD and Scrapie Require Agent-Associated Nucleic Acids for Infection.

Sotirios Botsios1, Laura Manuelidis1

  • 1Department of Surgery, Section of Neuropathology, Yale Medical School, New Haven, 06510, Connecticut.

Journal of Cellular Biochemistry
|January 17, 2016
PubMed
Summary

Transmissible Spongiform Encephalopathies (TSEs) are infectious diseases caused by replicating particles. New research shows these agents require nucleic acids, challenging the prion protein-only hypothesis for TSEs.

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Virulence profile: Laura Manuelidis.

Virulence·2016

Area of Science:

  • Neurovirology
  • Infectious Diseases
  • Molecular Biology

Background:

  • Transmissible Spongiform Encephalopathies (TSEs) are neurodegenerative diseases distinct from Alzheimer's.
  • TSEs are caused by infectious agents, unlike other neurodegenerative diseases.
  • The prevailing hypothesis attributes TSE strains to host prion protein (PrP) without genetic material.

Purpose of the Study:

  • To investigate the role of nucleic acids in TSE agent infectivity.
  • To challenge the prion-only hypothesis for TSE pathogenesis.
  • To determine if TSE agents require genetic material for replication and transmission.

Main Methods:

  • Development of rapid infectivity assays to isolate TSE particles.
  • Separation of infectious particles from host components, including PrP.
Keywords:
ALZHEIMER'S DISEASEGENOMEMICROBIOMENEURODEGENERATIONPRION AMYLOIDSPHINX DNAsVIRAL STRAINS

Related Experiment Videos

  • Exposure of TSE agents (FU-CJD and 22L scrapie) to nucleases in GT1 neuronal cells.

    • Main Results:

    • Digesting PrP did not reduce brain particle titers.
    • Nuclease treatment reproducibly reduced TSE agent infectivity by ≥99%.
    • Protected mitochondrial and circular SPHINX DNAs were destroyed by nucleases, while PrP remained unaltered.

    Conclusions:

    • TSE agents require protected genetic material to infect hosts.
    • These findings necessitate the reopening of investigations into essential agent nucleic acids.
    • The study provides evidence against the prion-only hypothesis and supports a viral or nucleic acid-based etiology for TSEs.