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Borna disease--neuropathology and pathogenesis

G Gosztonyi1, H Ludwig

  • 1Institut für Neuropathologie, Freie Universität Berlin, Universitätsklinikum Benjamin Franklin, Germany.

Current Topics in Microbiology and Immunology
|January 1, 1995
PubMed
Summary

West Nile virus causes nonpurulent encephalitis in animals, affecting the brain. Persistent infections in rats show absent inflammation but lead to neuronal degeneration, learning deficits, and obesity syndromes.

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Area of Science:

  • Veterinary Neurology
  • Neurovirology
  • Pathology

Background:

  • Bornavirus (BD) causes acute/subacute encephalitis in horses and sheep, primarily affecting gray matter in the olfactory, limbic, and brain stem regions.
  • Experimental BD can be induced across various animal species, from birds to primates, with neuropathology mirroring natural infections but showing more diffuse inflammation.

Purpose of the Study:

  • To investigate the neuropathological and clinical manifestations of Bornavirus (BD) infection in various animal models.
  • To elucidate the mechanisms of viral spread, antigen production, and the development of chronic sequelae, including learning deficits and obesity syndromes.

Main Methods:

  • Induction of experimental Bornavirus (BD) infection in a range of animal models, including rats, mice, birds, and primates.
  • Histopathological examination of nervous system tissues to identify viral antigen distribution, neuronal and glial cell involvement, and inflammatory responses.
  • Observation and characterization of clinical signs, including neurological deficits and the development of obesity syndromes in persistently infected rats.

Main Results:

  • Experimental BD infection in rats and mice can lead to persistent/tolerant infections lacking overt inflammation but characterized by focal degeneration in the dentate gyrus, retina, and hippocampus, correlating with learning and behavioral changes.
  • Viral antigens are abundantly produced and fill neuronal processes in all infected species; both neurons and glial cells are infected.
  • A subset of rats surviving acute BD infection develop an obesity syndrome, potentially linked to hypothalamic and hippocampal damage.

Conclusions:

  • Bornavirus (BD) infection causes significant neuropathology, including neuronal degeneration and inflammation, leading to neurological and behavioral deficits.
  • Persistent BD infections can occur without overt inflammation, highlighting distinct pathogenic mechanisms.
  • The study identifies potential anatomical substrates for learning deficiencies and neuroendocrine syndromes associated with BD infection, underscoring the complexity of viral pathogenesis in the central nervous system.

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