Demonstration of Borna disease virus (BDV) in specific regions of the brain from horses positive for serum antibodies to BDV but negative for BDV RNA in the blood and internal organs

1997 ◽  
Vol 186 (1) ◽  
pp. 19-24 ◽  
Author(s):  
Katsuro Hagiwara ◽  
Noriko Momiyama ◽  
Hiroyuki Taniyama ◽  
Takaaki Nakaya ◽  
Nobuo Tsunoda ◽  
...  
Keyword(s):  
Disease Virus ◽  
Serum Antibodies ◽  
Internal Organs ◽  
Borna Disease Virus ◽  
The Brain ◽  
Borna Disease

scholarly journals CD8 T Cells Require Gamma Interferon To Clear Borna Disease Virus from the Brain and Prevent Immune System-Mediated Neuronal Damage

2005 ◽  
Vol 79 (21) ◽  
pp. 13509-13518 ◽  
Author(s):  
Jürgen Hausmann ◽  
Axel Pagenstecher ◽  
Karen Baur ◽  
Kirsten Richter ◽  
Hanns-Joachim Rziha ◽  
...  
Keyword(s):  
T Cells ◽  
Disease Virus ◽  
Cd8 T Cells ◽  
Gamma Interferon ◽  
Wild Type ◽  
Borna Disease Virus ◽  
Ifn Γ ◽  
The Brain ◽  
Deficient Mice ◽  
Borna Disease

ABSTRACT Borna disease virus (BDV) frequently causes meningoencephalitis and fatal neurological disease in young but not old mice of strain MRL. Disease does not result from the virus-induced destruction of infected neurons. Rather, it is mediated by H-2 k -restricted antiviral CD8 T cells that recognize a peptide derived from the BDV nucleoprotein N. Persistent BDV infection in mice is not spontaneously cleared. We report here that N-specific vaccination can protect wild-type MRL mice but not mutant MRL mice lacking gamma interferon (IFN-γ) from persistent infection with BDV. Furthermore, we observed a significant degree of resistance of old MRL mice to persistent BDV infection that depended on the presence of CD8 T cells. We found that virus initially infected hippocampal neurons around 2 weeks after intracerebral infection but was eventually cleared in most wild-type MRL mice. Unexpectedly, young as well as old IFN-γ-deficient MRL mice were completely susceptible to infection with BDV. Moreover, neurons in the CA1 region of the hippocampus were severely damaged in most diseased IFN-γ-deficient mice but not in wild-type mice. Furthermore, large numbers of eosinophils were present in the inflamed brains of IFN-γ-deficient mice but not in those of wild-type mice, presumably because of increased intracerebral synthesis of interleukin-13 and the chemokines CCL1 and CCL11, which can attract eosinophils. These results demonstrate that IFN-γ plays a central role in host resistance against infection of the central nervous system with BDV and in clearance of BDV from neurons. They further indicate that IFN-γ may function as a neuroprotective factor that can limit the loss of neurons in the course of antiviral immune responses in the brain.

scholarly journals Virus-Specific CD4+ T Cells Eliminate Borna Disease Virus from the Brain via Induction of Cytotoxic CD8+T Cells

1998 ◽  
Vol 72 (5) ◽  
pp. 4387-4395 ◽  
Author(s):  
Kerstin Nöske ◽  
Thomas Bilzer ◽  
Oliver Planz ◽  
Lothar Stitz
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Line ◽  
Disease Virus ◽  
Target Cells ◽  
Borna Disease Virus ◽  
Infected Control ◽  
Low Level ◽  
The Brain ◽  
Borna Disease

ABSTRACT Persistent Borna disease virus infection of the brain can be prevented by treatment of naive rats with a virus-specific CD4+ T-cell line prior to infection. In rats receiving this treatment, only a transient low-level encephalitis was seen compared to an increasingly inflammatory reaction in untreated infected control rats. Virus replication was found in the brain for several days after infection before the virus was cleared from the central nervous system. The loss of infectivity from the brain was confirmed by negative results by reverse transcription-PCR with primers for mRNA, by in situ hybridization for both genomic and mRNA, and by immunohistology. Most importantly, in vitro assays revealed that the T-cell line used for transfusion had no cytotoxic capacity. The kinetics of virus clearance were paralleled by the appearance of CD8+ T cells and the expression of perforin in the brain. Testing of lymphocytes isolated from the brains of CD4+T-cell-treated rats after challenge revealed high cytotoxic activity due to the presence of CD8+ cytotoxic T cells at time points when brain lymphocytes from infected control rats induced low-level cytolysis of target cells. Neutralizing antiviral antibodies and gamma interferon were shown not to be involved in the elimination of virus from the brain.

scholarly journals Distribution of Borna Disease Virus in the Brain of Rats Infected with an Obesity-inducing Virus Strain

2006 ◽  
Vol 10 (1) ◽  
pp. 39-48 ◽  
Author(s):  
C. Herden ◽  
S. Herzog ◽  
J. A. Richt ◽  
A. Nesseler ◽  
M. Christ ◽  
...  
Keyword(s):  
Disease Virus ◽  
Virus Strain ◽  
Borna Disease Virus ◽  
The Brain ◽  
Borna Disease

MRI in psychiatric patients with serum antibodies against Borna disease virus

1989 ◽  
Vol 29 (3) ◽  
pp. 281-282 ◽  
Author(s):  
K. Bechter ◽  
S. Herzog ◽  
R. Schüttler ◽  
R. Rott
Keyword(s):  
Disease Virus ◽  
Psychiatric Patients ◽  
Serum Antibodies ◽  
Borna Disease Virus ◽  
Borna Disease

High-avidity human serum antibodies recognizing linear epitopes of borna disease virus proteins

2002 ◽  
Vol 51 (12) ◽  
pp. 979-987 ◽  
Author(s):  
Christian Billich ◽  
Christian Sauder ◽  
Ronald Frank ◽  
Sibylle Herzog ◽  
Karl Bechter ◽  
...  
Keyword(s):  
Human Serum ◽  
Disease Virus ◽  
High Avidity ◽  
Serum Antibodies ◽  
Borna Disease Virus ◽  
Linear Epitopes ◽  
Borna Disease ◽  
Virus Proteins

scholarly journals Borna Disease Virus Phosphoprotein Binds a Neurite Outgrowth Factor, Amphoterin/HMG-1

2001 ◽  
Vol 75 (18) ◽  
pp. 8742-8751 ◽  
Author(s):  
Wataru Kamitani ◽  
Yuko Shoya ◽  
Takeshi Kobayashi ◽  
Makiko Watanabe ◽  
Byeong-Jae Lee ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Disease Virus ◽  
Cell Lines ◽  
Cultured Cells ◽  
Borna Disease Virus ◽  
P24 Protein ◽  
Infected Cells ◽  
The Brain ◽  
Borna Disease

ABSTRACT The Borna disease virus (BDV) p24 phosphoprotein is an abundant protein in BDV-infected cultured cells and animal brains. Therefore, there is a possibility that binding of the p24 protein to cellular factor(s) induces functional alterations of infected neural cells in the brain. To identify a cellular protein(s) that interacts with BDV p24 protein, we performed far-Western blotting with extracts from various cell lines. Using recombinant p24 protein as a probe, we detected a 30-kDa protein in all cell lines examined. Binding between the 30-kDa and BDV p24 proteins was also demonstrated using BDV p24 affinity and ion-exchange chromatography columns. Microsequence analysis of the purified 30-kDa protein revealed that its N terminus showed complete homology with rat amphoterin protein, which is a neurite outgrowth factor abundant in the brain during development. Mammalian two-hybrid and immunoprecipitation analyses also confirmed that amphoterin is a specific target for the p24 protein in vivo. Furthermore, we showed that infection by BDV, as well as purified p24 protein in the medium, significantly decreased cell process outgrowth of cells grown on laminin, indicating the functional inhibition of amphoterin by interaction with the p24 protein. Immunohistochemical analysis revealed decreased levels of amphoterin protein at the leading edges of BDV-infected cells. Moreover, the expression of the receptor for advanced glycation end products, of which the extracellular moiety is a receptor for amphoterin, was not significantly activated in BDV-infected cells during the process of extension, suggesting that the secretion of amphoterin from the cell surface is inhibited by the binding of the p24 protein. These results suggested that BDV infection may cause direct damage in the developing brain by inhibiting the function of amphoterin due to binding by the p24 phosphoprotein.

Expression of interferon gamma in the brain of cats with natural Borna disease virus infection

2011 ◽  
Vol 141 (1-2) ◽  
pp. 162-167 ◽  
Author(s):  
Jonas Johansson Wensman ◽  
Carolina Ilbäck ◽  
Elina Hjertström ◽  
Anne-Lie Blomström ◽  
Malin Hagberg Gustavsson ◽  
...  
Keyword(s):  
Virus Infection ◽  
Disease Virus ◽  
Interferon Gamma ◽  
Borna Disease Virus ◽  
The Brain ◽  
Borna Disease

scholarly journals Features of Borna disease virus reproduction in brain cells and laboratory diagnosis of infection

2019 ◽  
Vol 2019 (2) ◽  
pp. 21-24
Author(s):  
Константин Юров ◽  
Konstantin Yurov ◽  
Светлана Алексеенкова ◽  
Svetlana Alekseenkova
Keyword(s):  
Disease Virus ◽  
Present Report ◽  
Retrograde Transport ◽  
Laboratory Diagnosis ◽  
Experimental Models ◽  
Brain Cells ◽  
Borna Disease Virus ◽  
The Brain ◽  
Borna Disease

The Borna Disease Virus (BDV) is a non-segmented RNA-containing virus belonging to the Bornaviridae family. The pathogen causes progressive meningoencephalitis in animals of various types. Despite numerous studies, some stages of reproduction of Bornavirus remain poorly understood, in particular, receptor-mediated penetration, retrograde transport into the nucleus, assembly and release of the virion, etc. The present report presents the results of demonstrating studies that were aimed at following the immunoenzyme method, the distribution of the main protein BDV ― phosphoprotein P (p24) in the brain cells of naturally susceptible animals, compare nnye data with the results of a number of authors, made mainly in experimental models. Microscopic examination of histological sections of the brain tissue of horses and sheep treated with specific serum against p24 BDV in a light or luminescent microscope observed a specific color in the form of: small granules; diffuse fluorescence of the cytoplasm; larger granules, apparently due to aggregation of endosomes, for axon transportation; formations in the form of beads, demonstrating the transport of viral material along the axon. In vitro results were obtained indicating that it is possible to transport RNPs via a short path through cytoplasmic bridges. The presented results will allow a better understanding of the neuropathogenesis of Born's disease and improve the diagnosis of the disease.

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