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Pathogenesis of viral infections of the central nervous system
Head : Daniel Dunia
Scientific objective :
Research in our laboratory explores the mechanisms and consequences of viral persistence in the central nervous system (CNS). Our studies focus primarily on one negative-strand virus, the Borna disease virus (BDV), which enables decoding the molecular mechanisms whereby a virus can persist in the CNS and lead to altered brain function. It also provides a fascinating window into neuroscience and cell biology, resulting from the tight interplay between this virus and neurons.
Our aims :
Our current projects focus on examining the molecular mechanisms of viral spread in neurons, on the analysis of the selective interference with signaling or epigenetic pathways that govern neuronal survival or plasticity. We also examine the interaction of BDV with the host's immune response within the CNS, with a particular focus on the antiviral CD8 T cell response an its resulting impact on neuronal physiology.
Main publications :
Chevalier G, Suberbielle E, Monnet C, Duplan V, Martin-Blondel G, Farrugia F, Le Masson G, Liblau R, Gonzalez-Dunia D
Neurons are MHC Class I-Dependent Targets for CD8 T Cells upon Neurotropic Viral Infection.
PLoS Pathog., 2011 Nov;7(11):e1002393. Epub 2011 Nov 17.
Prat CM, Schmid S, Farrugia F, Cenac N, Le Masson G, Schwemmle M, Gonzalez-Dunia D.
Mutation of the protein kinase C site in borna disease virus phosphoprotein abrogates viral interference with neuronal signaling and restores normal synaptic activity.
PLoS Pathog., 2009 May;5(5):e1000425. Epub 2009 May 8.
Suberbielle E, Stella A, Pont F, Monnet C, Mouton E, Lamouroux L, Monsarrat B, Gonzalez-Dunia D.
Proteomic analysis reveals selective impediment of neuronal remodeling upon Borna disease virus infection.
J Virol., 2008 Dec;82(24):12265-79. Epub 2008 Oct 1.
Volmer R, Prat CM, Le Masson G, Garenne A, Gonzalez-Dunia D.
Borna disease virus infection impairs synaptic plasticity.
J Virol. 2007, 2007 Aug;81(16):8833-7. Epub 2007 Jun 6.
Volmer R, Monnet C, Gonzalez-Dunia D.
Borna disease virus blocks potentiation of presynaptic activity through inhibition of protein kinase C signaling.
PLoS Pathog. 2006 Mar;2(3):e19. Epub 2006 Mar 17.
Neurons are MHC Class I-Dependent Targets for CD8 T Cells upon Neurotropic Viral Infection.
PLoS Pathog., 2011 Nov;7(11):e1002393. Epub 2011 Nov 17.
Prat CM, Schmid S, Farrugia F, Cenac N, Le Masson G, Schwemmle M, Gonzalez-Dunia D.
Mutation of the protein kinase C site in borna disease virus phosphoprotein abrogates viral interference with neuronal signaling and restores normal synaptic activity.
PLoS Pathog., 2009 May;5(5):e1000425. Epub 2009 May 8.
Suberbielle E, Stella A, Pont F, Monnet C, Mouton E, Lamouroux L, Monsarrat B, Gonzalez-Dunia D.
Proteomic analysis reveals selective impediment of neuronal remodeling upon Borna disease virus infection.
J Virol., 2008 Dec;82(24):12265-79. Epub 2008 Oct 1.
Volmer R, Prat CM, Le Masson G, Garenne A, Gonzalez-Dunia D.
Borna disease virus infection impairs synaptic plasticity.
J Virol. 2007, 2007 Aug;81(16):8833-7. Epub 2007 Jun 6.
Volmer R, Monnet C, Gonzalez-Dunia D.
Borna disease virus blocks potentiation of presynaptic activity through inhibition of protein kinase C signaling.
PLoS Pathog. 2006 Mar;2(3):e19. Epub 2006 Mar 17.
Date of update December 2, 2011
Version française
The team
Key words
Virus
Central nervous system
Neuronal signaling
Behavior
Synaptic plasticity
Central nervous system
Neuronal signaling
Behavior
Synaptic plasticity
Expected health effects
The remarkable features of BDV pathogenesis make it a very valuable tool to gain insight on the pathogenesis of many human neurological diseases. In particular, its predominant tropism for limbic structures in the brain, notably cortex and hippocampus, together with the diversity of symptoms triggered by BDV persistence constitute a fascinating model of viral interaction with the brain. A better understanding of the underlying mechanisms may provide new physiopathological clues for a better understanding of many human neurological diseases of unclear etiology.
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