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W. Ian Lipkin - One of the best experts on this subject based on the ideXlab platform.
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Borna Disease virus - fact and fantasy.
Virus research, 2011Co-Authors: W. Ian Lipkin, Thomas Briese, Mady HornigAbstract:The occasion of Brian Mahy's retirement as editor of Virus Research provides an opportunity to reflect on the work that led one of the authors (Lipkin) to meet him shortly after the molecular discovery and characterization of Borna Disease virus in the late 1980s, and work with authors Briese and Hornig to investigate mechanisms of pathogenesis and its potential role in human Disease. This article reviews the history, molecular biology, epidemiology, and pathobiology of Bornaviruses.
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Borna Disease virus
Journal of NeuroVirology, 2003Co-Authors: Mady Hornig, Thomas Briese, W. Ian LipkinAbstract:Borna Disease virus, a negative-strand RNA virus, infects a wide variety of warm-blooded animals. Depending on the age of the host and the integrity of its immune response, infection may be asymptomatic or cause a broad spectrum of behavioral disorders. Unusual features of Borna Disease virus biology include nuclear localization of replication and transcription; diverse strategies for regulation of gene expression; and interaction with signaling pathways resulting in subtle neuropathology. Although the question of human infection remains unresolved, burgeoning interest in this unique pathogen has provided tools for exploring the pharmacology and neurochemistry of neuropsychiatric disorders potentially linked to infection. Analysis of rodent models of infection has yielded insights into mechanisms by which neurotropic agents and/or immune factors may impact developing or mature central nervous system circuitry to effect complex disturbances in movement and behavior.
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Borna Disease virus.
Reviews in medical virology, 2001Co-Authors: Ingo Jordan, W. Ian LipkinAbstract:Borna Disease virus (BDV) is unique amongst animal RNA viruses in its molecular biology and capacity to cause persistent, noncytolytic CNS-infection in a wide variety of host species. Unlike other non-segmented negative-strand RNA animal viruses, BDV replicates in the nucleus of the host cell where splicing is employed for expression of a very compact genome. Epidemiological studies indicate a broad host range and geographical distribution, and some investigators have proposed that human infection may result in neuropsychiatric disorders. Experimental Borna Disease in neonatal and adult rats provides an intriguing model for immune-mediated disturbances of brain development and function.
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Borna Disease virus and neuropsychiatric Disease – a reappraisal
Trends in microbiology, 2001Co-Authors: W. Ian Lipkin, Mady Hornig, Thomas BrieseAbstract:Abstract Despite progress in understanding the molecular biology and pathobiology of Borna Disease virus, its epidemiology and role in human Disease remain controversial. The challenges encountered in this field are a paradigm for the investigation of Diseases potentially linked to complex host–microorganism interactions.
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Inhibition of Borna Disease virus replication by ribavirin.
Journal of virology, 1999Co-Authors: Ingo Jordan, Thomas Briese, Devron R. Averett, W. Ian LipkinAbstract:The guanosine analogue ribavirin was tested for antiviral activity in two neural cell lines, human oligodendrocytes and rat glia, against Borna Disease virus (BDV) strains V and He/80. Ribavirin treatment resulted in lower levels of virus and viral transcripts within 12 h. Addition of guanosine but not adenosine resulted in a profound reduction of the ribavirin effect. Ribavirin appears to be an effective antiviral agent for treatment of BDV infection in vitro. A likely mechanism for its activity is reduction of the intracellular GTP pool, resulting in inhibition of transcription and capping of BDV mRNAs.
Thomas Briese - One of the best experts on this subject based on the ideXlab platform.
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Borna Disease virus - fact and fantasy.
Virus research, 2011Co-Authors: W. Ian Lipkin, Thomas Briese, Mady HornigAbstract:The occasion of Brian Mahy's retirement as editor of Virus Research provides an opportunity to reflect on the work that led one of the authors (Lipkin) to meet him shortly after the molecular discovery and characterization of Borna Disease virus in the late 1980s, and work with authors Briese and Hornig to investigate mechanisms of pathogenesis and its potential role in human Disease. This article reviews the history, molecular biology, epidemiology, and pathobiology of Bornaviruses.
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Borna Disease virus
Journal of NeuroVirology, 2003Co-Authors: Mady Hornig, Thomas Briese, W. Ian LipkinAbstract:Borna Disease virus, a negative-strand RNA virus, infects a wide variety of warm-blooded animals. Depending on the age of the host and the integrity of its immune response, infection may be asymptomatic or cause a broad spectrum of behavioral disorders. Unusual features of Borna Disease virus biology include nuclear localization of replication and transcription; diverse strategies for regulation of gene expression; and interaction with signaling pathways resulting in subtle neuropathology. Although the question of human infection remains unresolved, burgeoning interest in this unique pathogen has provided tools for exploring the pharmacology and neurochemistry of neuropsychiatric disorders potentially linked to infection. Analysis of rodent models of infection has yielded insights into mechanisms by which neurotropic agents and/or immune factors may impact developing or mature central nervous system circuitry to effect complex disturbances in movement and behavior.
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Borna Disease virus and neuropsychiatric Disease a reappraisal
Trends in Microbiology, 2001Co-Authors: Ian W Lipkin, Mady Hornig, Thomas BrieseAbstract:Abstract Despite progress in understanding the molecular biology and pathobiology of Borna Disease virus, its epidemiology and role in human Disease remain controversial. The challenges encountered in this field are a paradigm for the investigation of Diseases potentially linked to complex host–microorganism interactions.
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Borna Disease virus and neuropsychiatric Disease – a reappraisal
Trends in microbiology, 2001Co-Authors: W. Ian Lipkin, Mady Hornig, Thomas BrieseAbstract:Abstract Despite progress in understanding the molecular biology and pathobiology of Borna Disease virus, its epidemiology and role in human Disease remain controversial. The challenges encountered in this field are a paradigm for the investigation of Diseases potentially linked to complex host–microorganism interactions.
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Inhibition of Borna Disease virus replication by ribavirin.
Journal of virology, 1999Co-Authors: Ingo Jordan, Thomas Briese, Devron R. Averett, W. Ian LipkinAbstract:The guanosine analogue ribavirin was tested for antiviral activity in two neural cell lines, human oligodendrocytes and rat glia, against Borna Disease virus (BDV) strains V and He/80. Ribavirin treatment resulted in lower levels of virus and viral transcripts within 12 h. Addition of guanosine but not adenosine resulted in a profound reduction of the ribavirin effect. Ribavirin appears to be an effective antiviral agent for treatment of BDV infection in vitro. A likely mechanism for its activity is reduction of the intracellular GTP pool, resulting in inhibition of transcription and capping of BDV mRNAs.
L Stitz - One of the best experts on this subject based on the ideXlab platform.
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Prevention of Virus Persistence and Protection against Immunopathology after Borna Disease Virus Infection of the Brain by a Novel Orf Virus Recombinant
Journal of virology, 2005Co-Authors: Marco Henkel, L Stitz, Oliver Planz, Timo Fischer, Hanns-joachim RzihaAbstract:The Parapoxvirus Orf virus represents a promising candidate for novel vector vaccines due to its immune modulating properties even in nonpermissive hosts such as mouse or rat. The highly attenuated Orf virus strain D1701 was used to generate a recombinant virus (D1701-VrVp40) expressing nucleoprotein p40 of Borna Disease virus, which represents a major antigen for the induction of a Borna Disease virus-specific humoral and cellular immune response. Infection with Borna Disease virus leads to distinct neurological symptoms mediated by the invasion of activated specific CD8+ T cells into the infected brain. Usually, Borna Disease virus is not cleared from the brain but rather persists in neural cells. In the present study we show for the first time that intramuscular application of the D1701-VrVp40 recombinant protected rats against Borna Disease, and importantly, virus clearance from the infected brain was demonstrated in immunized animals. Even 4 and 8 months after the last immunization, all immunized animals were still protected against the Disease. Initial characterization of the immune cells attracted to the infected brain areas suggested that D1701-VrVp40 mediated induction of B cells and antibody-producing plasma cells as well as T cells. These findings suggest the induction of various defense mechanisms against Borna Disease virus. First studies on the role of antiviral cytokines indicated that D1701-VrVp40 immunization did not lead to an enhanced early response of gamma or alpha interferon or tumor necrosis factor alpha. Collectively, this study describes the potential of the Orf virus vector system in mediating long-lasting, protective antiviral immunity and eliminating this persistent virus infection without provoking massive neuronal damage.
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Borna Disease Virus Nucleoprotein Interacts with the Cdc2-Cyclin B1 Complex
Journal of virology, 2003Co-Authors: Oliver Planz, L Stitz, Stephan Pleschka, Katja Oesterle, Friederike Berberich-siebelt, Christina Ehrhardt, Stephan LudwigAbstract:Transition from G2 to M phase, a cell cycle checkpoint, is regulated by the Cdc2-cyclin B1 complex. Here, we report that persistent infection with Borna Disease virus (BDV), a noncytolytic RNA virus infecting the central nervous system, results in decelerated proliferation of infected host cells due to a delayed G2-to-M transition. Persistent BDV-infected rat fibroblast cells showed reduced proliferation compared to uninfected cells. In pull-down assays we observed an interaction of the viral nucleoprotein with the Cdc2-cyclin B1 complex. Transfection of the viral nucleoprotein but not of the phosphoprotein also results in decelerated proliferation. This phenomenon was found in BDV-susceptible primary rat fibroblast cells and also in primary mouse cells, which are not susceptible to BDV infection. This is the first evidence that the noncytolytic Borna Disease virus can manipulate host cell functions via interaction of the viral nucleoprotein with mitotic entry regulators. BDV preferentially infects and persists in nondividing neurons. The present report could give an explanation for this selective choice of host cell by BDV.
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The immunopathogenesis of Borna Disease virus infection.
Frontiers in bioscience : a journal and virtual library, 2002Co-Authors: L Stitz, Thomas Bilzer, Oliver PlanzAbstract:Borna Disease virus (BDV) infection represents an excellent model system to study immunopathological mechanisms based on a T cell-mediated immune reaction in the central nervous system. The single-stranded RNA Borna Disease virus, a member of Bornaviridae in the order of Mononegavirale, lacks cytopathogenicity both in vitro and in vivo. After experimental infection BDV causes a persistent infection of the central nervous system and induces Borna Disease, an immune-mediated encephalomyelitis. The infiltrating immune cells have been characterized as CD4-positive, CD8-positive T-cells, macrophages and B cells. CD8-positive T cells represent the effector cell population exhibiting antigen specificity for the nucleoprotein.
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Lack of antiviral effect of amantadine in Borna Disease virus infection
Medical microbiology and immunology, 1998Co-Authors: L Stitz, Oliver Planz, Thomas BilzerAbstract:The antiviral effect of amantadine (1-aminoadamantane) was tested in vitro as well as in vivo. Treatment of persistently Borna Disease virus (BDV)-infected cell lines of different origin and for various length of time did not result in a general reduction of virus titer or clearance of virus from infected cells. In vivo, rats were treated with amantadine by daily oral application or by use of osmotic pumps, and in both cases treatment was started before infection. Neither route of application of the drug had any influence on the time of onset of Disease, on antiviral antibody titers, on virus titer in the brain, on the severity of the inflammatory reaction in the brain, or on the severity of neurological symptoms. These experiments, although revealing negative results and obtained using a virus from a natural case of Borna Disease grown after isolation in vitro for a long period of time, should caution from the general use of amantadine as a curative agent against BDV infection as has been implicated recently [Bode et al. (1997) Lancet 349:178-179].
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Neutralizing antibodies in Borna Disease virus-infected rats.
Journal of virology, 1995Co-Authors: Carolyn G. Hatalski, S Kliche, L Stitz, W I LipkinAbstract:Borna Disease is a neurologic syndrome caused by infection with a nonsegmented, negative-strand RNA virus, Borna Disease virus. Infected animals have antibodies to two soluble viral proteins, p40 and p23, and a membrane-associated viral glycoprotein, gp18. We examined the time course for the development of neutralization activity and the expression of antibodies to individual viral proteins in sera of infected rats. The appearance of neutralizing activity correlated with the development of immunoreactivity to gp18, but not p40 or p23. Monospecific and monoclonal antibodies to native gp18 and recombinant nonglycosylated gp18 were also found to have neutralizing activity and to immunoprecipitate viral particles or subparticles. These findings suggest that gp18 is likely to be present on the surface of the viral particles and is likely to contain epitopes important for virus neutralization.
Kathryn M. Carbone - One of the best experts on this subject based on the ideXlab platform.
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Borna Disease virus (BDV)-induced model of autism: application to vaccine safety test design.
Molecular Psychiatry, 2002Co-Authors: Kathryn M. Carbone, S. A. Rubin, Mikhail V. PletnikovAbstract:Borna Disease virus (BDV)-induced model of autism: application to vaccine safety test design
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Borna Disease Virus And Its Role In Neurobehavioral Disease
2002Co-Authors: Kathryn M. CarboneAbstract:Table of Contents 1. Borna Disease Virus: Spanning a Century of Science, Keizo Tomonaga and Kathryn M. Carbone 2. Borna Disease Virus Molecular Virology, Masahiko Kishi, Keizo Tomonaga, Patrick Lai, and Juan Carlos de la Torre 3. Laboratory Diagnosis, Christian Sauder, Tetsuya Mizutani, and Kazunari Yamaguchi 4. Epidemiology and Infection of Natural Animal Hosts, Kazuyoshi Ikuta, Kasuro Hagiwara, Hiroyuki Taniyama, and Norbert Nowotny 5. Experimental Infection: Pathogenesis of Neurobehavioral Disease, Mikhail V. Pletnikov, Daniel Gonzalez-Dunia, and Lothar Stitz 6. Human Borna Disease Virus Infection, Oliver Planz, Karl Bechter, and Martin Scwemmle
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Borna Disease: virus-induced neurobehavioral Disease pathogenesis.
Current opinion in microbiology, 2001Co-Authors: Kathryn M. Carbone, Steven A. Rubin, Yoshii Nishino, Mikhail V. PletnikovAbstract:Abstract Studies of the pathogenesis of neurobehavioral Diseases following Borna Disease virus infections have been increasing rapidly over the past ten years. Recent major advances have included a report of vertical transmission of the virus in its natural host, the horse, and a report of isolation of a novel variant, No/98, in that same species. In rats infected neonatally with the Borna Disease virus that lack blood-borne inflammation in the brain, evidence of an ‘endogenous’ brain inflammatory response is abundant, with elevated expression of cytokine and chemokine mRNA. Infection in these rats is also associated with abnormal levels of neurotransmitters, including serotonin and norepinephrine. Data and debate continue to be forthcoming about the role of Borna Disease virus in human infection and psychiatric Disease.
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In vivo treatment with anti-α4 integrin suppresses clinical and pathological evidence of Borna Disease virus infection
Journal of neuroimmunology, 1998Co-Authors: S. A. Rubin, T.a Yednock, Kathryn M. CarboneAbstract:Abstract Borna Disease virus (BDV) infection of the rat brain induces a severe T-lymphocyte mediated inflammatory response that parallels the course of clinical Borna Disease. In other models of CNS inflammation, the recruitment of T-lymphocytes from the circulation to sites of inflammation is believed to be directed, in part, by the cellular adhesion molecules α 4 β 1 integrin (expressed on T-lymphocytes) and its ligand VCAM-1 (expressed on blood brain barrier endothelium). Since BDV-specific T-lymphocytes are known to express the α 4 β 1 integrin, we examined the effect of in vivo treatment with an anti- α 4 integrin monoclonal antibody (GG5/3) on the development of BDV-specific encephalitis and Borna Disease. Here, we report that the inhibition of α 4 integrin provided significant clinical benefit in slowing the progression of Borna Disease. Antibody treatment greatly reduced the immune cell infiltrates in the CNS of BDV-infected animals, but we found that this inhibition of the immune response did not result in enhanced viral levels.
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Borna Disease virus in mice: host-specific differences in Disease expression.
Journal of virology, 1993Co-Authors: S. A. Rubin, R W Waltrip, J R Bautista, Kathryn M. CarboneAbstract:We developed a mouse model of Borna Disease to facilitate immunopathogenesis research by adaptation of Borna Disease virus to mice through serial passage in mouse brain tissue. Borna Disease virus replication, antibody production, inflammation, and Borna Disease expression in several different strains of mice were examined.
Mingju Wang - One of the best experts on this subject based on the ideXlab platform.
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Borna Disease virus infection perturbs energy metabolites and amino acids in cultured human oligodendroglia cells
PLOS ONE, 2012Co-Authors: Rongzhong Huang, Hongchang Gao, Liang Zhang, Jianmin Jia, Xia Liu, Peng Zheng, Jing Deng, Xiao Wang, Liu Yang, Mingju WangAbstract:BACKGROUND Borna Disease virus is a neurotropic, non-cytolytic virus that has been widely employed in neuroscientific research. Previous studies have revealed that metabolic perturbations are associated with Borna Disease viral infection. However, the pathophysiological mechanism underlying its mode of action remains unclear. METHODOLOGY Human oligodendroglia cells infected with the human strain Borna Disease virus Hu-H1 and non-infected matched control cells were cultured in vitro. At day 14 post-infection, a proton nuclear magnetic resonance-based metabonomic approach was used to differentiate the metabonomic profiles of 28 independent intracellular samples from Borna Disease virus-infected cells (n = 14) and matched control cells (n = 14). Partial least squares discriminant analysis was performed to demonstrate that the whole metabonomic patterns enabled discrimination between the two groups, and further statistical testing was applied to determine which individual metabolites displayed significant differences between the two groups. FINDINGS Metabonomic profiling revealed perturbations in 23 metabolites, 19 of which were deemed individually significant: nine energy metabolites (α-glucose, acetate, choline, creatine, formate, myo-inositol, nicotinamide adenine dinucleotide, pyruvate, succinate) and ten amino acids (aspartate, glutamate, glutamine, glycine, histidine, isoleucine, phenylalanine, threonine, tyrosine, valine). Partial least squares discriminant analysis demonstrated that the whole metabolic patterns enabled statistical discrimination between the two groups. CONCLUSION Borna Disease viral infection perturbs the metabonomic profiles of several metabolites in human oligodendroglia cells cultured in vitro. The findings suggest that Borna Disease virus manipulates the host cell's metabolic network to support viral replication and proliferation.