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Juan Carlos De La Torre - One of the best experts on this subject based on the ideXlab platform.

  • Reverse-genetic approaches to the study of Borna Disease Virus
    Nature Reviews Microbiology, 2006
    Co-Authors: Juan Carlos De La Torre
    Abstract:

    This article outlines the recently developed reverse-genetics systems for Borna Disease Virus (BDV), which will provide a powerful tool for the investigation of the cis -acting signals and trans -acting factors that control BDV RNA replication and gene expression. Borna Disease Virus (BDV) is an enveloped Virus that has a non-segmented, negative-strand RNA genome with the characteristic organization of the mononegaViruses. However, based on its unique genetic and biological features, BDV is considered to be the prototypic member of a new mononegaVirus family, the Bornaviridae . BDV causes central nervous system (CNS) Disease in a wide variety of mammals. This article discusses the recently developed reverse-genetics systems for BDV, and the implications for the elucidation of the molecular mechanisms underlying BDV–host interactions, including the basis of BDV persistence in the CNS and its associated Diseases.

  • Reverse-genetic approaches to the study of Borna Disease Virus.
    Nature reviews. Microbiology, 2006
    Co-Authors: Juan Carlos De La Torre
    Abstract:

    Borna Disease Virus (BDV) is an enveloped Virus that has a non-segmented, negative-strand RNA genome with the characteristic organization of the mononegaViruses. However, based on its unique genetic and biological features, BDV is considered to be the prototypic member of a new mononegaVirus family, the Bornaviridae. BDV causes central nervous system (CNS) Disease in a wide variety of mammals. This article discusses the recently developed reverse-genetics systems for BDV, and the implications for the elucidation of the molecular mechanisms underlying BDV-host interactions, including the basis of BDV persistence in the CNS and its associated Diseases.

  • synaptic pathology in Borna Disease Virus persistent infection
    Journal of Virology, 2000
    Co-Authors: Daniel Gonzalezdunia, Sylvie Syan, Michiko Watanabe, Margaret Mallory, Eliezer Masliah, Juan Carlos De La Torre
    Abstract:

    Borna Disease Virus (BDV) infection of newborn rats leads to a persistent infection of the brain, which is associated with behavioral and neuroanatonomical abnormalities. These disorders occur in the absence of lymphoid cell infiltrates, and BDV-induced cell damage is restricted to defined brain areas. To investigate if damage to synaptic structures anteceded neuronal loss in BDV neonatally infected rats, we analyzed at different times postinfection the expression levels of growth-associated protein 43 and synaptophysin, two molecules involved in neuroplasticity processes. We found that BDV induced a progressive and marked decrease in the expression of these synaptic markers, which was followed by a significant loss of cortical neurons. Our findings suggest that BDV persistent infection interferes with neuroplasticity processes in specific cell populations. This, in turn, could affect the proper supply of growth factors and other molecules required for survival of selective neuronal populations within the cortex and limbic system structures.

  • Borna Disease Virus and the brain.
    Brain research bulletin, 1997
    Co-Authors: Daniel Gonzalez–dunia, Christian Sauder, Juan Carlos De La Torre
    Abstract:

    Viruses with the ability to establish persistent infection in the central nervous system (CNS) can induce progressive neurologic disorders associated with diverse pathological manifestations. Clinical, epidemiological, and virological evidence supports the hypothesis that Viruses contribute to human mental Diseases whose etiology remains elusive. Therefore, the investigation of the mechanisms whereby Viruses persist in the CNS and disturb normal brain function represents an area of research relevant to clinical and basic neurosciences. Borna Disease Virus (BDV) causes CNS Disease in several vertebrate species characterized by behavioral abnormalities. Based on its unique features, BDV represents the prototype of a new Virus family. BDV provides an important model for the investigation of the mechanisms and consequences of viral persistence in the CNS. The BDV paradigm is amenable to study Virus-cell interactions in the CNS that can lead to neurodevelopmental abnormalities, immune-mediated damage, as well as alterations in cell differentiated functions that affect brain homeostasis. Moreover, seroepidemiological data and recent molecular studies indicate that BDV is associated with certain neuropsychiatric Diseases. The potential role of BDV and of other yet to be uncovered BDV-related Viruses in human mental health provides additional impetus for the investigation of this novel neurotropic infectious agent.

Thomas Briese - One of the best experts on this subject based on the ideXlab platform.

  • Borna Disease Virus - fact and fantasy.
    Virus research, 2011
    Co-Authors: W. Ian Lipkin, Thomas Briese, Mady Hornig
    Abstract:

    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.

  • Borna Disease Virus
    Journal of NeuroVirology, 2003
    Co-Authors: Mady Hornig, Thomas Briese, W. Ian Lipkin
    Abstract:

    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.

  • Borna Disease Virus and neuropsychiatric Disease a reappraisal
    Trends in Microbiology, 2001
    Co-Authors: Ian W Lipkin, Mady Hornig, Thomas Briese
    Abstract:

    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.

  • Borna Disease Virus and neuropsychiatric Disease – a reappraisal
    Trends in microbiology, 2001
    Co-Authors: W. Ian Lipkin, Mady Hornig, Thomas Briese
    Abstract:

    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.

  • Inhibition of Borna Disease Virus replication by ribavirin.
    Journal of virology, 1999
    Co-Authors: Ingo Jordan, Thomas Briese, Devron R. Averett, W. Ian Lipkin
    Abstract:

    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.

W I Lipkin - One of the best experts on this subject based on the ideXlab platform.

  • Orofacial dyskinesias and dystonia in rats infected with Borna Disease Virus; a model for tardive dyskinetic syndromes.
    Molecular psychiatry, 1999
    Co-Authors: Marylou V. Solbrig, George F. Koob, W I Lipkin
    Abstract:

    The neurochemical and lesion effects of Borna Disease Virus infection in rats result in a syndrome with phenotypic and pharmacological similarities to tardive dyskinesia.

  • Naloxone-induced seizures in rats infected with Borna Disease Virus.
    Neurology, 1996
    Co-Authors: Marylou V. Solbrig, George F. Koob, W I Lipkin
    Abstract:

    The opioid antagonist naloxone is widely used in the emergency treatment of nontraumatic coma. Although it is uncommon for serious side effects to result from administration of opiate antagonists, we report that naloxone can have epileptogenic effects in the context of encephalitis. In an experimental model of viral encephalitis, rats infected with Borna Disease Virus developed myoclonic, generalized clonic, or atonic seizures; behavior arrest; and staring spells when treated with naloxone. These findings suggest a novel neuropharmacologic link, through opioid peptide systems, between epilepsy and encephalitis and disclose a potential contraindication to use of opioid antagonists in nontraumatic coma.

  • Characterization of the Borna Disease Virus phosphoprotein, p23.
    Journal of virology, 1996
    Co-Authors: S Kliche, Thomas Briese, L Stitz, Harry Mangalam, L Shi, Thomas Binz, H Niemann, W I Lipkin
    Abstract:

    Borna Disease Virus infection is diagnosed by the presence of serum antibodies reactive with the major viral proteins, p40 and p23. Although p40 and p23 are unrelated in amino acid sequence structure, cross-reactive antibodies are described. Protein fragments and synthetic peptides were analyzed to characterize the specificities of antibodies to p23. Epitope mapping revealed eight continuous epitopes accessible on the surface of a predicted structural model for the monomeric and the disulfide-linked dimeric forms of p23. None of these epitopes was reactive with antibodies to p40. Cross-reactivity with monospecific sera and monoclonal antibodies to p40 was found for one discontinuous epitope located at the amino terminus of p23.

  • Enzyme-linked immunosorbent assay for detecting antibodies to Borna Disease Virus-specific proteins.
    Journal of clinical microbiology, 1995
    Co-Authors: Thomas Briese, Yoo-sun Park, Carolyn G. Hatalski, S Kliche, W I Lipkin
    Abstract:

    Borna Disease Virus is a unique neurotropic RNA Virus that causes neurologic Disease in a wide variety of animal hosts. We established an enzyme-linked immunosorbent assay for the detection of antibodies to Borna Disease Virus on the basis of the use of three recombinant viral proteins (recp40, recp23, and recp18). This assay system is more sensitive and rapid than the methods currently used for the serologic diagnosis of infection such as Western blotting (immunoblotting), indirect immunofluorescence test, or immunoprecipitation.

  • Neutralizing antibodies in Borna Disease Virus-infected rats.
    Journal of virology, 1995
    Co-Authors: Carolyn G. Hatalski, S Kliche, L Stitz, W I Lipkin
    Abstract:

    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.

W. Ian Lipkin - One of the best experts on this subject based on the ideXlab platform.

  • Borna Disease Virus - fact and fantasy.
    Virus research, 2011
    Co-Authors: W. Ian Lipkin, Thomas Briese, Mady Hornig
    Abstract:

    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.

  • Borna Disease Virus
    Journal of NeuroVirology, 2003
    Co-Authors: Mady Hornig, Thomas Briese, W. Ian Lipkin
    Abstract:

    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.

  • Borna Disease Virus.
    Reviews in medical virology, 2001
    Co-Authors: Ingo Jordan, W. Ian Lipkin
    Abstract:

    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.

  • Borna Disease Virus and neuropsychiatric Disease – a reappraisal
    Trends in microbiology, 2001
    Co-Authors: W. Ian Lipkin, Mady Hornig, Thomas Briese
    Abstract:

    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.

  • Inhibition of Borna Disease Virus replication by ribavirin.
    Journal of virology, 1999
    Co-Authors: Ingo Jordan, Thomas Briese, Devron R. Averett, W. Ian Lipkin
    Abstract:

    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.

Kathryn M. Carbone - One of the best experts on this subject based on the ideXlab platform.

  • Borna Disease Virus (BDV)-induced model of autism: application to vaccine safety test design.
    Molecular Psychiatry, 2002
    Co-Authors: Kathryn M. Carbone, S. A. Rubin, Mikhail V. Pletnikov
    Abstract:

    Borna Disease Virus (BDV)-induced model of autism: application to vaccine safety test design

  • Borna Disease Virus And Its Role In Neurobehavioral Disease
    2002
    Co-Authors: Kathryn M. Carbone
    Abstract:

    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

  • Borna Disease: Virus-induced neurobehavioral Disease pathogenesis.
    Current opinion in microbiology, 2001
    Co-Authors: Kathryn M. Carbone, Steven A. Rubin, Yoshii Nishino, Mikhail V. Pletnikov
    Abstract:

    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.

  • Borna Disease Virus and human Disease
    Clinical Microbiology Reviews, 2001
    Co-Authors: Kathryn M. Carbone
    Abstract:

    The biology of Borna Disease Virus (BDV) strongly supports the likelihood of human infection with BDV or a variant of BDV. Thus far, the evidence supporting BDV infection in humans has initiated much controversy among basic and clinical scientists; only time and additional research will support or refute the hypothesis of human BDV infection. Until an assay of acceptable specificity and sensitivity has been developed, validated, and used to document human BDV infection, scientists cannot reasonably begin to associate BDV infection with specific Disease syndromes. Clinical studies seeking causal associations between BDV infection and specific Diseases must ensure the proper identification of the BDV infection status of patients and control subjects by using a validated, highly sensitive, and highly specific assay (or series of assays). For clinical studies, a highly sensitive “screening” test followed by a highly specific confirmatory test will be of significant benefit. Although it is possible to formulate hypotheses about the clinical outcomes of human BDV infection based on animal model work, to date no human Disease has been causally linked to human BDV infection. Scientists all over the world are actively pursuing these issues, and with continuing advances in clinical and basic BDV research, the answers cannot be far away.

  • Borna Disease Virus antibodies and the deficit syndrome of schizophrenia
    Schizophrenia research, 1997
    Co-Authors: Royce W. Waltrip, Steven A. Rubin, Robert W. Buchanan, William T. Carpenter, Brian Kirkpatrick, Ann Summerfelt, Alan Breier, Kathryn M. Carbone
    Abstract:

    We detected anti-Borna Disease Virus (BDV) antibodies at a 14.4% rate in patients with schizophrenia. The hypothesis of a higher rate of BDV seropositivity in deficit syndrome was borne out in a subset of 64 patients categorized according to the Schedule for the Deficit Syndrome with 5/15 seropositive deficit and 4/49 seropositive nondeficit (p < 0.05). This suggests that the antibodies and possibly a BDV-like Virus are pathogenetically linked to this form of schizophrenia.