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Related Experiment Videos

Transmissible encephalopathies: speculations and realities.

Laura Manuelidis1

  • 1Yale Medical School, New Haven, Connecticut 06510, USA. laura.manuelidis@yale.edu

Viral Immunology
|June 28, 2003
PubMed
Summary

Transmissible spongiform encephalopathies (TSEs) may not be caused by prions alone. Evidence suggests an infectious agent, possibly viral, copurifies with nucleic acids and replicates before prion protein abnormalities appear.

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Virulence profile: Laura Manuelidis.

Virulence·2016

Area of Science:

  • Neuroscience
  • Virology
  • Biochemistry

Background:

  • Transmissible spongiform encephalopathies (TSEs) like CJD, BSE, and scrapie are enigmatic neurodegenerative diseases.
  • The dominant prion hypothesis posits that misfolded prion protein (PrP) alone causes TSEs.
  • This hypothesis faces challenges due to experimental evidence.

Purpose of the Study:

  • To critically evaluate the prion hypothesis for TSE pathogenesis.
  • To present evidence questioning the sufficiency of prion protein in TSE.
  • To explore alternative explanations for TSE causation.

Main Methods:

  • Review of diverse experimental findings challenging the prion-only hypothesis.
  • Analysis of data on infectious agent composition, size, and replication kinetics.
  • Examination of host immune responses and agent strain characteristics.

Main Results:

  • Infectious agents in TSEs copurify with nucleic acids and separate from most PrP.
  • The infectious particle exhibits viral-like size (~25 nm) and is sensitive to disruption of viral components.
  • Replication of the infectious agent precedes detectable PrP abnormalities, suggesting PrP changes are a host response.

Conclusions:

  • The prion hypothesis is inconsistent with experimental data.
  • Evidence supports an infectious agent, likely viral, as the cause of TSEs.
  • PrP abnormalities are likely a pathological host response, not the infectious agent itself.

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