Neurotransmitter abnormalities in Borna disease

@article{Lipkin1988NeurotransmitterAI,
  title={Neurotransmitter abnormalities in Borna disease},
  author={W. Ian Lipkin and Kathryn M. Carbone and Michael C. Wilson and Cynthia S. Duchala and Opendra Narayan and Michael B. A. Oldstone},
  journal={Brain Research},
  year={1988},
  volume={475},
  pages={366-370}
}
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Borna disease virus: molecular analysis of a neurotropic infectious agent.
Borna Disease Virus and the Brain
Experimental Infection: Pathogenesis of Neurobehavioral Disease
TLDR
Investigations of experimental adult BDV infection in other species replicated findings from the rat model and extended one's understanding of the pathogenesis of BD, where the virus replication was predominantly detected in the cerebral cortex and hippocampus.
Borna Disease Virus Persistence Causes Inhibition of Glutamate Uptake by Feline Primary Cortical Astrocytes
TLDR
Evidence is presented that BDV can establish a nonlytic chronic infection in primary cortical feline astrocytes that is associated with a severe impairment in the astroCytes' ability to uptake glutamate, and findings suggest that, in vivo, BDV could also affect an importantAstrocyte function required to prevent neuronal excitotoxicity.
Borna disease--neuropathology and pathogenesis.
TLDR
In the acute disease, inflammatory reaction can severely aggravate virus-induced cytopathology, but cannot be the sole cause of the neurological disease, since infection with high passage virus can lead to a similarly severe disease in the absence of inflammatory changes.
Neuropharmacological sequelae of persistent CNS viral infections: lessons from Borna Disease Virus
Disturbance of the Cortical Cholinergic Innervation in Borna Disease Prior to Encephalitis
TLDR
The motor, mood, learning and memory disabilities in BDV‐infected rats are likely to result, in part, from cortical cholinergic denervation, giving new insights into the pathogenesis of neurological disease caused by a noncytopathogenic virus.
Molecular characterization of the Borna disease agent.
Borna disease virus infection of adult and neonatal rats: models for neuropsychiatric disease.
TLDR
Findings in this chapter support the relevance of BDV infections of neonatal Lewis rats as models for investigating mechanisms of neurodevelopmental damage in autism.
Upregulation of COX-2 and CGRP Expression in Resident Cells of the Borna Disease Virus-Infected Brain Is Dependent upon Inflammation
TLDR
Increased CGRP and COX-2 expression in the BDV-infected brain is the result of the inflammatory response and likely to be involved in the pathogenesis of virus-induced encephalitis.
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References

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The frenzied behavior and subsequent blindness in immunocompetent adults were attributed to a uniquely transient immunopathologic reaction targeted to centers in the limbic system and retinal neurons.
Pathogenesis of Borna disease in rats: evidence that intra-axonal spread is the major route for virus dissemination and the determinant for disease incubation
TLDR
The incubation period is the time required for transport of the agent in dendritic-axonal processes from the site of inoculation to the hippocampus and the exclusiveness of the neural conduit was proven by failure to cause infection after injection of the virus intravenously or into the feet of neurectomized rats.
Viral infection of neurons can depress neurotransmitter mRNA levels without histologic injury
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LIGHT MICROSCOPE AND IMMUNOHISTOLOGICAL INVESTIGATIONS ON THE BRAIN OF BORNA DISEASE VIRUS‐INFECTED RABBITS
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There was a meningeal inflammatory reaction together with perivenous cellular infiltrates which were most numerous in the sti actures of the limbic system and basal ganglia, but also prominent in the spinal ganglia and area postrema.
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It is demonstrated that neonatal rats can acquire a persistent, tolerant infection and that expression of disease is mediated by immunological factors.
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