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  1. Article ; Online: La phosphoprotéine P du virus de la maladie de Borna altère le développement des neurones GABAergiques humains.

    Scordel, Chloé / Coulpier, Muriel

    Medecine sciences : M/S

    2015  Volume 31, Issue 12, Page(s) 1060–1063

    Title translation The Borna disease virus phosphoprotein alters the development of human GABAergic neurons.
    MeSH term(s) Borna disease virus/physiology ; Cell Proliferation ; GABAergic Neurons/cytology ; GABAergic Neurons/virology ; Humans ; Phosphoproteins/physiology ; Viral Proteins/physiology
    Chemical Substances Phosphoproteins ; Viral Proteins
    Language French
    Publishing date 2015-12
    Publishing country France
    Document type News
    ZDB-ID 632733-3
    ISSN 1958-5381 ; 0767-0974
    ISSN (online) 1958-5381
    ISSN 0767-0974
    DOI 10.1051/medsci/20153112003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Borna disease virus phosphoprotein impairs the developmental program controlling neurogenesis and reduces human GABAergic neurogenesis.

    Scordel, Chloé / Huttin, Alexandra / Cochet-Bernoin, Marielle / Szelechowski, Marion / Poulet, Aurélie / Richardson, Jennifer / Benchoua, Alexandra / Gonzalez-Dunia, Daniel / Eloit, Marc / Coulpier, Muriel

    PLoS pathogens

    2015  Volume 11, Issue 4, Page(s) e1004859

    Abstract: It is well established that persistent viral infection may impair cellular function of specialized cells without overt damage. This concept, when applied to neurotropic viruses, may help to understand certain neurologic and neuropsychiatric diseases. ... ...

    Abstract It is well established that persistent viral infection may impair cellular function of specialized cells without overt damage. This concept, when applied to neurotropic viruses, may help to understand certain neurologic and neuropsychiatric diseases. Borna disease virus (BDV) is an excellent example of a persistent virus that targets the brain, impairs neural functions without cell lysis, and ultimately results in neurobehavioral disturbances. Recently, we have shown that BDV infects human neural progenitor cells (hNPCs) and impairs neurogenesis, revealing a new mechanism by which BDV may interfere with brain function. Here, we sought to identify the viral proteins and molecular pathways that are involved. Using lentiviral vectors for expression of the bdv-p and bdv-x viral genes, we demonstrate that the phosphoprotein P, but not the X protein, diminishes human neurogenesis and, more particularly, GABAergic neurogenesis. We further reveal a decrease in pro-neuronal factors known to be involved in neuronal differentiation (ApoE, Noggin, TH and Scg10/Stathmin2), demonstrating that cellular dysfunction is associated with impairment of specific components of the molecular program that controls neurogenesis. Our findings thus provide the first evidence that a viral protein impairs GABAergic human neurogenesis, a process that is dysregulated in several neuropsychiatric disorders. They improve our understanding of the mechanisms by which a persistent virus may interfere with brain development and function in the adult.
    MeSH term(s) Active Transport, Cell Nucleus ; Apolipoproteins E/antagonists & inhibitors ; Apolipoproteins E/metabolism ; Biomarkers/chemistry ; Biomarkers/metabolism ; Borna Disease/metabolism ; Borna Disease/pathology ; Borna Disease/virology ; Borna disease virus/physiology ; Carrier Proteins/antagonists & inhibitors ; Carrier Proteins/metabolism ; Cell Proliferation ; Cells, Cultured ; Down-Regulation ; France ; GABAergic Neurons/cytology ; GABAergic Neurons/metabolism ; GABAergic Neurons/pathology ; GABAergic Neurons/virology ; Host-Pathogen Interactions ; Human Embryonic Stem Cells/cytology ; Human Embryonic Stem Cells/metabolism ; Human Embryonic Stem Cells/pathology ; Human Embryonic Stem Cells/virology ; Humans ; Membrane Proteins/antagonists & inhibitors ; Membrane Proteins/metabolism ; Nerve Tissue Proteins/antagonists & inhibitors ; Nerve Tissue Proteins/metabolism ; Neurogenesis ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Recombinant Proteins/metabolism ; Recombinant Proteins/toxicity ; Tyrosine 3-Monooxygenase/antagonists & inhibitors ; Tyrosine 3-Monooxygenase/metabolism ; Viral Structural Proteins/genetics ; Viral Structural Proteins/metabolism
    Chemical Substances Apolipoproteins E ; Biomarkers ; Carrier Proteins ; Membrane Proteins ; Nerve Tissue Proteins ; P protein, Borna disease virus ; Phosphoproteins ; Recombinant Proteins ; STMN2 protein, human ; Viral Structural Proteins ; noggin protein (148294-77-3) ; Tyrosine 3-Monooxygenase (EC 1.14.16.2)
    Language English
    Publishing date 2015-04-29
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2205412-1
    ISSN 1553-7374 ; 1553-7366
    ISSN (online) 1553-7374
    ISSN 1553-7366
    DOI 10.1371/journal.ppat.1004859
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Borna disease virus phosphoprotein impairs the developmental program controlling neurogenesis and reduces human GABAergic neurogenesis.

    Chloé Scordel / Alexandra Huttin / Marielle Cochet-Bernoin / Marion Szelechowski / Aurélie Poulet / Jennifer Richardson / Alexandra Benchoua / Daniel Gonzalez-Dunia / Marc Eloit / Muriel Coulpier

    PLoS Pathogens, Vol 11, Iss 4, p e

    2015  Volume 1004859

    Abstract: It is well established that persistent viral infection may impair cellular function of specialized cells without overt damage. This concept, when applied to neurotropic viruses, may help to understand certain neurologic and neuropsychiatric diseases. ... ...

    Abstract It is well established that persistent viral infection may impair cellular function of specialized cells without overt damage. This concept, when applied to neurotropic viruses, may help to understand certain neurologic and neuropsychiatric diseases. Borna disease virus (BDV) is an excellent example of a persistent virus that targets the brain, impairs neural functions without cell lysis, and ultimately results in neurobehavioral disturbances. Recently, we have shown that BDV infects human neural progenitor cells (hNPCs) and impairs neurogenesis, revealing a new mechanism by which BDV may interfere with brain function. Here, we sought to identify the viral proteins and molecular pathways that are involved. Using lentiviral vectors for expression of the bdv-p and bdv-x viral genes, we demonstrate that the phosphoprotein P, but not the X protein, diminishes human neurogenesis and, more particularly, GABAergic neurogenesis. We further reveal a decrease in pro-neuronal factors known to be involved in neuronal differentiation (ApoE, Noggin, TH and Scg10/Stathmin2), demonstrating that cellular dysfunction is associated with impairment of specific components of the molecular program that controls neurogenesis. Our findings thus provide the first evidence that a viral protein impairs GABAergic human neurogenesis, a process that is dysregulated in several neuropsychiatric disorders. They improve our understanding of the mechanisms by which a persistent virus may interfere with brain development and function in the adult.
    Keywords Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
    Subject code 616
    Language English
    Publishing date 2015-04-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article: Borna disease virus phosphoprotein impairs the developmental program controlling neurogenesis and reduces human GABAergic neurogenesis

    Scordel, Chloé / Huttin, Alexandra / Cochet Bernoin, Marielle / Szelechowski, Marion / Poulet, Aurélie / Richardson, Jennifer / Benchoua, Alexandra / Gonzalez-Dunia, Daniel / Eloit, Marc / Coulpier, Muriel

    Plos Pathogens 4 (11), . (2015)

    Abstract: It is well established that persistent viral infection may impair cellular function of specialized cells without overt damage. This concept, when applied to neurotropic viruses, may help to understand certain neurologic and neuropsychiatric diseases. ... ...

    Abstract It is well established that persistent viral infection may impair cellular function of specialized cells without overt damage. This concept, when applied to neurotropic viruses, may help to understand certain neurologic and neuropsychiatric diseases. Borna disease virus (BDV) is an excellent example of a persistent virus that targets the brain, impairs neural functions without cell lysis, and ultimately results in neurobehavioral disturbances. Recently, we have shown that BDV infects human neural progenitor cells (hNPCs) and impairs neurogenesis, revealing a new mechanism by which BDV may interfere with brain function. Here, we sought to identify the viral proteins and molecular pathways that are involved. Using lentiviral vectors for expression of the bdv-p and bdv-x viral genes, we demonstrate that the phosphoprotein P, but not the X protein, diminishes human neurogenesis and, more particularly, GABAergic neurogenesis. We further reveal a decrease in pro-neuronal factors known to be involved in neuronal differentiation (ApoE, Noggin, TH and Scg10/Stathmin2), demonstrating that cellular dysfunction is associated with impairment of specific components of the molecular program that controls neurogenesis. Our findings thus provide the first evidence that a viral protein impairs GABAergic human neurogenesis, a process that is dysregulated in several neuropsychiatric disorders. They improve our understanding of the mechanisms by which a persistent virus may interfere with brain development and function in the adult.
    Language English
    Document type Article
    Database AGRIS - International Information System for the Agricultural Sciences and Technology

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  5. Article: Borna disease virus phosphoprotein impairs the developmental program controlling neurogenesis and reduces human GABAergic neurogenesis

    Scordel, Chloé / Huttin, Alexandra / Cochet Bernoin, Marielle / Szelechowski, Marion / Poulet, Aurélie / Richardson, Jennifer / Benchoua, Alexandra / Gonzalez-Dunia, Daniel / Eloit, Marc / Coulpier, Muriel

    Plos Pathogens 4 (11), . (2015)

    Abstract: It is well established that persistent viral infection may impair cellular function of specialized cells without overt damage. This concept, when applied to neurotropic viruses, may help to understand certain neurologic and neuropsychiatric diseases. ... ...

    Abstract It is well established that persistent viral infection may impair cellular function of specialized cells without overt damage. This concept, when applied to neurotropic viruses, may help to understand certain neurologic and neuropsychiatric diseases. Borna disease virus (BDV) is an excellent example of a persistent virus that targets the brain, impairs neural functions without cell lysis, and ultimately results in neurobehavioral disturbances. Recently, we have shown that BDV infects human neural progenitor cells (hNPCs) and impairs neurogenesis, revealing a new mechanism by which BDV may interfere with brain function. Here, we sought to identify the viral proteins and molecular pathways that are involved. Using lentiviral vectors for expression of the bdv-p and bdv-x viral genes, we demonstrate that the phosphoprotein P, but not the X protein, diminishes human neurogenesis and, more particularly, GABAergic neurogenesis. We further reveal a decrease in pro-neuronal factors known to be involved in neuronal differentiation (ApoE, Noggin, TH and Scg10/Stathmin2), demonstrating that cellular dysfunction is associated with impairment of specific components of the molecular program that controls neurogenesis. Our findings thus provide the first evidence that a viral protein impairs GABAergic human neurogenesis, a process that is dysregulated in several neuropsychiatric disorders. They improve our understanding of the mechanisms by which a persistent virus may interfere with brain development and function in the adult.
    Language English
    Document type Article
    Database AGRIS - International Information System for the Agricultural Sciences and Technology

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