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Peripheral and intracerebral T cell immune response in cats naturally infected with Borna disease virus

Borna disease virus (BDV) is a neurotropic agent with capacity to cause encephalomyelitis in a wide range of animal species, including horses and cats. Recent studies also point to a link between BDV and human neuropsychiatric disorders. The pathogenesis of Borna disease (BD) has been proposed to be...

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Main Authors: Berg, Anna-Lena (Author) , Johannisson, A. (Author) , Johansson, M. (Author) , Hein, Andreas (Author) , Berg, M. (Author) , Dörries, Rüdiger (Author)
Format: Article (Journal)
Language:English
Published: 2 June 1999
In: Veterinary immunology and immunopathology
Year: 1999, Volume: 68, Issue: 2, Pages: 241-253
ISSN:1873-2534
DOI:10.1016/S0165-2427(99)00030-6
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/S0165-2427(99)00030-6
Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S0165242799000306
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Author Notes:A-L Berg, A. Johannisson, M. Johansson, A. Hein, M. Berg, R. Dörries
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Summary:Borna disease virus (BDV) is a neurotropic agent with capacity to cause encephalomyelitis in a wide range of animal species, including horses and cats. Recent studies also point to a link between BDV and human neuropsychiatric disorders. The pathogenesis of Borna disease (BD) has been proposed to be immune-mediated, mainly through the effects of cytotoxic T cells. We used flow cytometric analysis in order to characterize the peripheral and intracerebral T cell immune response in cats naturally infected with BDV. Our results show the presence of two different CD8+ cell populations (CD8+low and CD8+high) in the blood, spleen and brain of these cats. In the brain, CD8+low cells predominated over CD8+high cells. Since CD8+low cells have been suggested to represent a non-MHC-restricted T cell population, the recruitment of such cells to the brains of BDV-infected cats could possibly be of importance for the clearance of virus from neurones.
Item Description:Gesehen am 30.06.2022
Physical Description:Online Resource
ISSN:1873-2534
DOI:10.1016/S0165-2427(99)00030-6

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