Pathogenesis of Borna disease.
Abstract: Borna disease represents a unique model of a virus-induced immunological disease of the brain. Naturally occurring in horses and sheep, the mechanisms of pathogenesis have been studied in experimental animals, namely in the rat. Many investigations have revealed that the infection of the natural hosts principally follows the same pathogenic pathways as observed in rats, leading to a severe encephalomyelitis. This affliction of the central nervous system results in severe neurological disorders that again, are fully comparable in laboratory animals to those in the natural and the different experimental hosts. In addition, alterations have been reported which are also based on the infection of the brain and do not result in the classical encephalitic clinical picture but rather in alterations of behavior. However, to all of our knowledge, the various clinical pictures of Borna disease are not caused by the infecting virus itself but rather by the hosts immune response towards it, i.e. by a virus-induced cell-mediated immunopathological reaction. The importance of virus-specific CD4+ T cells as exemplified by a cultured T cell line and of CD8+ T cells as shown by immunomodulatory substances and specific antibody treatment in vivo for the pathogenesis of acute Borna disease will be elucidated here. In addition, evidence will be provided that virus-specific CD8+ T cells are also responsible for the dramatic brain atrophy in the chronic phase of the disease in rats. Therefore, Borna disease not only lends itself exquisitely well to the study of the pathogenesis of an immunopathological disease of the brain but also represents one of the few models for immune-mediated tissue destruction that eventually leads to brain atrophy and clinically to dementia.
Publication Date: 1993-01-01 PubMed ID: 8219798DOI: 10.1007/978-3-7091-9300-6_11Google Scholar: Lookup
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- Journal Article
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Summary
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This research investigates Borna disease, a virus-triggered immunological brain disease that commonly occurs in horses and sheep. The study reveals that the illness is caused not directly by the virus, but the host’s immune response towards it. The paper particularly focuses on roles of specific T cells in disease pathology and how they contribute to brain atrophy and clinical dementia.
Understanding Borna Disease
- Borna disease is a unique kind of virus-induced immunological illness that primarily affects the brain.
- It primarily occurs in horses and sheep, but the pathogenesis – or the mechanism by which the disease develops – is also studied in laboratory rats.
- This disease leads to serious brain and spinal cord inflammation known as encephalomyelitis, which results in severe neurological disorders. These conditions in lab animals are comparable to those seen in the natural hosts.
- Interestingly, some modifications have been reported based on brain infection, leading to behavioural alterations instead of the typical clinical picture of encephalitis.
Role of Virus and Host’s Immune Response
- According to findings, the diverse clinical signs of Borna disease are not directly caused by the infecting virus.
- Rather, the disease is caused by the host’s immune reaction to it, described as a virus-induced, cell-mediated immunopathological reaction.
- This finding suggests a new aspect of viral infections where the immune response of the host plays a more significant role in disease manifestation than the virus itself.
T Cells in Borna Disease Pathogenesis
- The research emphasizes the importance of virus-specific CD4+ and CD8+ T cells in the pathogenesis of acute Borna disease.
- The study provides robust evidence that virus-specific CD8+ T cells are responsible for the severe brain atrophy observed in the chronic phase of the disease in rats.
Implications of the Study
- Besides offering a model for studying pathogenesis of immunopathological diseases of the brain, Borna disease illustrates the concept of immune-mediated tissue destruction.
- It provides a model of how these processes can ultimately lead to brain atrophy and clinical dementia, offering valuable insights for treatment interventions and strategies.
Cite This Article
APA
Stitz L, Bilzer T, Richt JA, Rott R.
(1993).
Pathogenesis of Borna disease.
Arch Virol Suppl, 7, 135-151.
https://doi.org/10.1007/978-3-7091-9300-6_11 Publication
Researcher Affiliations
- Institut für Virologie, Justus-Liebig-Universität, Giessen, Federal Republic of Germany.
MeSH Terms
- Animals
- Borna Disease / etiology
- Borna Disease / immunology
- Borna Disease / pathology
- Borna disease virus / immunology
- Borna disease virus / physiology
- Humans
Citations
This article has been cited 11 times.- . Bornavirus : Stellungnahmen des Arbeitskreises Blut des Bundesministeriums für Gesundheit.. Bundesgesundheitsblatt Gesundheitsforschung Gesundheitsschutz 2019 Apr;62(4):519-532.
- Chevalier G, Suberbielle E, Monnet C, Duplan V, Martin-Blondel G, Farrugia F, Le Masson G, Liblau R, Gonzalez-Dunia D. Neurons are MHC class I-dependent targets for CD8 T cells upon neurotropic viral infection.. PLoS Pathog 2011 Nov;7(11):e1002393.
- Wünschmann A, Honkavuori K, Briese T, Lipkin WI, Shivers J, Armien AG. Antigen tissue distribution of Avian bornavirus (ABV) in psittacine birds with natural spontaneous proventricular dilatation disease and ABV genotype 1 infection.. J Vet Diagn Invest 2011 Jul;23(4):716-26.
- Gray P, Hoppes S, Suchodolski P, Mirhosseini N, Payne S, Villanueva I, Shivaprasad HL, Honkavuori KS, Lipkin WI, Briese T, Reddy SM, Tizard I. Use of avian bornavirus isolates to induce proventricular dilatation disease in conures.. Emerg Infect Dis 2010 Mar;16(3):473-9.
- Rinder M, Ackermann A, Kempf H, Kaspers B, Korbel R, Staeheli P. Broad tissue and cell tropism of avian bornavirus in parrots with proventricular dilatation disease.. J Virol 2009 Jun;83(11):5401-7.
- Honkavuori KS, Shivaprasad HL, Williams BL, Quan PL, Hornig M, Street C, Palacios G, Hutchison SK, Franca M, Egholm M, Briese T, Lipkin WI. Novel borna virus in psittacine birds with proventricular dilatation disease.. Emerg Infect Dis 2008 Dec;14(12):1883-6.
- Schneider U, Ackermann A, Staeheli P. A Borna disease virus vector for expression of foreign genes in neurons of rodents.. J Virol 2007 Jul;81(13):7293-6.
- Iwata Y, Takahashi K, Peng X, Fukuda K, Ohno K, Ogawa T, Gonda K, Mori N, Niwa S, Shigeta S. Detection and sequence analysis of borna disease virus p24 RNA from peripheral blood mononuclear cells of patients with mood disorders or schizophrenia and of blood donors.. J Virol 1998 Dec;72(12):10044-9.
- Shoya Y, Kobayashi T, Koda T, Ikuta K, Kakinuma M, Kishi M. Two proline-rich nuclear localization signals in the amino- and carboxyl-terminal regions of the Borna disease virus phosphoprotein.. J Virol 1998 Dec;72(12):9755-62.
- Planz O, Bilzer T, Stitz L. Immunopathogenic role of T-cell subsets in Borna disease virus-induced progressive encephalitis.. J Virol 1995 Feb;69(2):896-903.
- Lundgren AL, Lindberg R, Ludwig H, Gosztonyi G. Immunoreactivity of the central nervous system in cats with a Borna disease-like meningoencephalomyelitis (staggering disease).. Acta Neuropathol 1995;90(2):184-93.
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