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Borna disease–neuropathology and pathogenesis.
Abstract: Natural BD is a nonpurulent acute/subacute encephalitis of horses and sheep with a propensity to involve the olfactory and limbic systems, and the brain stem. The inflammation is concentrated primarily in the gray matter, but subcortical white matter may also be affected. Experimental BD can be produced in a series of animals from birds to primates. The neuropathology after experimental infection is similar to that in natural disease but the inflammatory changes are more diffuse. In the rat and mouse, a persistent/tolerant infection can also be induced, in which inflammatory changes are conspicuously absent. In the course of persistent infection of the rat, an elective, focal degeneration ensues that involves the dentate gyrus, retina, and, less frequently, the magnocellular part of the hippocampus. The cytopathic destruction of the dentate gyrus is the likely anatomical substrate of learning deficiencies and behavioral changes, prominent features of chronic infection. Later in infection, more diffuse and random degeneration of neurons can be found. In all species infected, viral antigens are produced in excess and fill all neuronal processes. Beside neurons, glial cells are infected as well. The agent spreads in the nervous system axonally and transsynaptically (transneuronally). The type of neurotransmitter receptors in the synapse and their interaction with viral proteins may modulate the spread of infection (Gosztonyi et al. 1994). Virus particles have not been visualized in the brain in any phase of the disease. During persistent infection of the rat, production of viral proteins has a phasic character. Some rats survive acute infection and develop an obesity syndrome. The anatomical basis of this syndrome is not fully clarified; inflammatory destruction of the infundibular region, vacuolar degeneration of the paraventricular nucleus of the hypothalamus and severe, progressive involution of the hippocampal formation most probably play an important role in the production of this neuroendocrine syndrome. 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.
Publication Date: 1995-01-01 PubMed ID: 7789150 The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
- Journal Article
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- Non-U.S. Gov't
- Review
Summary
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The article investigates the neuropathology and pathogenesis of Borna disease, a type of encephalitis affecting animals like horses and sheep. The researchers look at how the disease affects different parts of the brains of various species, particularly those connected to learning and behavior, and explore possible mechanisms of its spread and progression.
Understanding Borna Disease
- The research begins by explaining Borna Disease (BD) as an acute to subacute form of encephalitis often found in horses and sheep. This essentially means it’s a sudden onset inflammation of the brain that commonly affects these particular animals.
- The inflammation, characterised by gray matter affliction and potential subcortical white matter involvement, prominently impacts the olfactory and limbic systems and the brain stem. This means the disease primarily affects areas of the brain responsible for smell, emotions, and basic life functions.
- Notably, the study states that BD can be experimentally induced in a range of animals covering birds to primates. In such scenarios, the neuropathology mirrors that of the natural disease, albeit with more spread-out inflammatory changes.
Virus Behavior in Different Animal Models
- In rats and mice, the scientists could induce a persistent infection where inflammatory changes were conspicuously missing. This means the virus was present and replicating, but the typical immune response was absent. This lead to focal degeneration in specific areas of the brain, including the dentate gyrus, retina, and—less frequently—the hippocampus. The resulting lesions were suggested as potential causes for deficient learning and behavioural changes often observed in chronically infected animals
- Later during infection, a more widespread and random degeneration of neurons could be noticed. Despite this widespread spread across various species, the researchers never visualized virus particles in any phase in the brain.
- In terms of the infection’s spread, it occurs axonally and transsynaptically, meaning it moves along nerve cells and across synapses, the communication points between neurons. The research suggests that the nature of the synaptic transmission and the interplay with viral proteins could influence this spread.
Additional Observations and Conclusions
- Coming to additional observations, the researchers noted that during persistent infection phases seen in rats, viral protein production follows a phasic pattern. Post-acute infection, some rats developed an obesity syndrome, possibly linked to inflammatory damage in parts of the hypothalamus and a progressive involution of the hippocampal formation.
- In acute disease stages, the inflammatory reaction can potentially worsen virus-induced cytopathology. However, inflammation alone cannot be attributed as the only cause of the neurological syndrome. This is because a similarly severe disease development can follow high-passage virus infections, which happen without accompanying inflammatory changes.
Cite This Article
APA
Gosztonyi G, Ludwig H.
(1995).
Borna disease–neuropathology and pathogenesis.
Curr Top Microbiol Immunol, 190, 39-73.
Publication
Researcher Affiliations
- Institut fu00fcr Neuropathologie, Freie Universitu00e4t Berlin, Universitu00e4tsklinikum Benjamin Franklin, Germany.
MeSH Terms
- Animals
- Antigens, Viral / analysis
- Borna Disease / etiology
- Borna Disease / immunology
- Borna Disease / pathology
- Borna disease virus / physiology
- Brain / pathology
- Humans
- Immunity, Cellular
- Neurons / pathology
- Viral Proteins / analysis
Citations
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