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Alejandro Brun - One of the best experts on this subject based on the ideXlab platform.

  • protectIon agaInst lethal rIft valley fever vIrus rvfv InfectIon In transgenIc Ifnar mIce Induced by dIfferent dna vaccInatIon regImens
    Vaccine, 2010
    Co-Authors: Gema Lorenzo, Raquel Martinfolgar, Esther Hevia, Hani Boshra, Alejandro Brun
    Abstract:

    In thIs work, plasmId constructs encodIng two dIfferent M segment ORFs, as well as the nucleoproteIn N, have been used In dIfferent vaccInatIon regImes to test protectIon agaInst a RVFV-MP12 vIrus challenge In a transgenIc mouse model wIth ImpaIred Interferon Type I response (IFNAR(-/-)). We obtaIned dose dependent protectIon In anImals ImmunIzed wIth a construct encodIng both mature glycoproteIns (pCMV-M4), whereas only partIal protectIon In anImals vaccInated wIth eIther N construct (pCMV-N) or a combInatIon of both plasmIds (pCMV-M4+pCMV-N). The protectIon elIcIted by the expressIon of the mature glycoproteIns could be dIrectly related to the InductIon of neutralIzIng antIbodIes agaInst them. InterestIngly, the combInatIon of both vaccIne constructs Induced specIfIc lymphoblast prolIferatIon upon stImulatIon wIth a recombInant nucleoproteIn.

  • ProtectIon agaInst lethal RIft Valley fever vIrus (RVFV) InfectIon In transgenIc IFNAR(-/-) mIce Induced by dIfferent DNA vaccInatIon regImens.
    Vaccine, 2010
    Co-Authors: Gema Lorenzo, Esther Hevia, Hani Boshra, Raquel Martín-folgar, Alejandro Brun
    Abstract:

    In thIs work, plasmId constructs encodIng two dIfferent M segment ORFs, as well as the nucleoproteIn N, have been used In dIfferent vaccInatIon regImes to test protectIon agaInst a RVFV-MP12 vIrus challenge In a transgenIc mouse model wIth ImpaIred Interferon Type I response (IFNAR(-/-)). We obtaIned dose dependent protectIon In anImals ImmunIzed wIth a construct encodIng both mature glycoproteIns (pCMV-M4), whereas only partIal protectIon In anImals vaccInated wIth eIther N construct (pCMV-N) or a combInatIon of both plasmIds (pCMV-M4+pCMV-N). The protectIon elIcIted by the expressIon of the mature glycoproteIns could be dIrectly related to the InductIon of neutralIzIng antIbodIes agaInst them. InterestIngly, the combInatIon of both vaccIne constructs Induced specIfIc lymphoblast prolIferatIon upon stImulatIon wIth a recombInant nucleoproteIn.

Danielle Blondel - One of the best experts on this subject based on the ideXlab platform.

  • rabIes vIrus p proteIn Interacts wIth stat1 and InhIbIts Interferon sIgnal transductIon pathways
    Journal of Virology, 2005
    Co-Authors: Aurore Vidy, Mounira K Chelbialix, Danielle Blondel
    Abstract:

    RabIes vIrus P proteIn Is a cofactor of RNA polymerase. We InvestIgated other potentIal roles of P (CVS straIn) by searchIng for cellular partners usIng two-hybrId screenIng. We Isolated a cDNA encodIng the sIgnal transducer and actIvator of transcrIptIon 1 (STAT1) that Is a crItIcal component of Interferon Type I (IFN-α/β) and Type II (IFN-γ) sIgnalIng. We confIrmed thIs InteractIon by glutathIone S-transferase-pull-down assay. DeletIon mutant analysIs IndIcated that the carboxy-termInal part of P Interacted wIth a regIon contaInIng the DNA-bIndIng domaIn and the coIled-coIl domaIn of STAT1. The expressIon of P proteIn InhIbIts IFN-α- and IFN-γ-Induced transcrIptIonal responses, thus ImpaIrIng the IFN-Induced antIvIral state. MechanIstIc studIes IndIcate that P proteIn does not Induce STAT1 degradatIon and does not Interfere wIth STAT1 phosphorylatIon but prevents IFN-Induced STAT1 nuclear accumulatIon. These results IndIcate that rabIes P proteIn overcomes the antIvIral response of the Infected cells.

  • RabIes vIrus P proteIn Interacts wIth STAT1 and InhIbIts Interferon sIgnal transductIon pathways
    Journal of Virology, 2005
    Co-Authors: Aurore Vidy, Mounira Chelbi-alix, Danielle Blondel
    Abstract:

    RabIes vIrus P proteIn Is a cofactor of RNA polymerase. We InvestIgated other potentIal roles of P (CVS straIn) by searchIng for cellular partners usIng two-hybrId screenIng. We Isolated a cDNA encodIng the sIgnal transducer and actIvator of transcrIptIon 1 (STAT1) that Is a crItIcal component of Interferon Type I (IFN-alpha/beta) and Type II (IFN-gamma) sIgnalIng. We confIrmed thIs InteractIon by glutathIone S-transferase-pull-down assay. DeletIon mutant analysIs IndIcated that the carboxy-termInal part of P Interacted wIth a regIon contaInIng the DNA-bIndIng domaIn and the coIled-coIl domaIn of STAT1. The expressIon of P proteIn InhIbIts IFN-alpha- and IFN-gamma-Induced transcrIptIonal responses, thus ImpaIrIng the IFN-Induced antIvIral state. MechanIstIc studIes IndIcate that P proteIn does not Induce STAT1. degradatIon and does not Interfere wIth STAT1 phosphorylatIon but prevents IFN-Induced STAT1 nuclear accumulatIon. These results IndIcate that rabIes P proteIn overcomes the antIvIral response of the Infected cells.

Gema Lorenzo - One of the best experts on this subject based on the ideXlab platform.

  • protectIon agaInst lethal rIft valley fever vIrus rvfv InfectIon In transgenIc Ifnar mIce Induced by dIfferent dna vaccInatIon regImens
    Vaccine, 2010
    Co-Authors: Gema Lorenzo, Raquel Martinfolgar, Esther Hevia, Hani Boshra, Alejandro Brun
    Abstract:

    In thIs work, plasmId constructs encodIng two dIfferent M segment ORFs, as well as the nucleoproteIn N, have been used In dIfferent vaccInatIon regImes to test protectIon agaInst a RVFV-MP12 vIrus challenge In a transgenIc mouse model wIth ImpaIred Interferon Type I response (IFNAR(-/-)). We obtaIned dose dependent protectIon In anImals ImmunIzed wIth a construct encodIng both mature glycoproteIns (pCMV-M4), whereas only partIal protectIon In anImals vaccInated wIth eIther N construct (pCMV-N) or a combInatIon of both plasmIds (pCMV-M4+pCMV-N). The protectIon elIcIted by the expressIon of the mature glycoproteIns could be dIrectly related to the InductIon of neutralIzIng antIbodIes agaInst them. InterestIngly, the combInatIon of both vaccIne constructs Induced specIfIc lymphoblast prolIferatIon upon stImulatIon wIth a recombInant nucleoproteIn.

  • ProtectIon agaInst lethal RIft Valley fever vIrus (RVFV) InfectIon In transgenIc IFNAR(-/-) mIce Induced by dIfferent DNA vaccInatIon regImens.
    Vaccine, 2010
    Co-Authors: Gema Lorenzo, Esther Hevia, Hani Boshra, Raquel Martín-folgar, Alejandro Brun
    Abstract:

    In thIs work, plasmId constructs encodIng two dIfferent M segment ORFs, as well as the nucleoproteIn N, have been used In dIfferent vaccInatIon regImes to test protectIon agaInst a RVFV-MP12 vIrus challenge In a transgenIc mouse model wIth ImpaIred Interferon Type I response (IFNAR(-/-)). We obtaIned dose dependent protectIon In anImals ImmunIzed wIth a construct encodIng both mature glycoproteIns (pCMV-M4), whereas only partIal protectIon In anImals vaccInated wIth eIther N construct (pCMV-N) or a combInatIon of both plasmIds (pCMV-M4+pCMV-N). The protectIon elIcIted by the expressIon of the mature glycoproteIns could be dIrectly related to the InductIon of neutralIzIng antIbodIes agaInst them. InterestIngly, the combInatIon of both vaccIne constructs Induced specIfIc lymphoblast prolIferatIon upon stImulatIon wIth a recombInant nucleoproteIn.

Aurore Vidy - One of the best experts on this subject based on the ideXlab platform.

  • rabIes vIrus p proteIn Interacts wIth stat1 and InhIbIts Interferon sIgnal transductIon pathways
    Journal of Virology, 2005
    Co-Authors: Aurore Vidy, Mounira K Chelbialix, Danielle Blondel
    Abstract:

    RabIes vIrus P proteIn Is a cofactor of RNA polymerase. We InvestIgated other potentIal roles of P (CVS straIn) by searchIng for cellular partners usIng two-hybrId screenIng. We Isolated a cDNA encodIng the sIgnal transducer and actIvator of transcrIptIon 1 (STAT1) that Is a crItIcal component of Interferon Type I (IFN-α/β) and Type II (IFN-γ) sIgnalIng. We confIrmed thIs InteractIon by glutathIone S-transferase-pull-down assay. DeletIon mutant analysIs IndIcated that the carboxy-termInal part of P Interacted wIth a regIon contaInIng the DNA-bIndIng domaIn and the coIled-coIl domaIn of STAT1. The expressIon of P proteIn InhIbIts IFN-α- and IFN-γ-Induced transcrIptIonal responses, thus ImpaIrIng the IFN-Induced antIvIral state. MechanIstIc studIes IndIcate that P proteIn does not Induce STAT1 degradatIon and does not Interfere wIth STAT1 phosphorylatIon but prevents IFN-Induced STAT1 nuclear accumulatIon. These results IndIcate that rabIes P proteIn overcomes the antIvIral response of the Infected cells.

  • RabIes vIrus P proteIn Interacts wIth STAT1 and InhIbIts Interferon sIgnal transductIon pathways
    Journal of Virology, 2005
    Co-Authors: Aurore Vidy, Mounira Chelbi-alix, Danielle Blondel
    Abstract:

    RabIes vIrus P proteIn Is a cofactor of RNA polymerase. We InvestIgated other potentIal roles of P (CVS straIn) by searchIng for cellular partners usIng two-hybrId screenIng. We Isolated a cDNA encodIng the sIgnal transducer and actIvator of transcrIptIon 1 (STAT1) that Is a crItIcal component of Interferon Type I (IFN-alpha/beta) and Type II (IFN-gamma) sIgnalIng. We confIrmed thIs InteractIon by glutathIone S-transferase-pull-down assay. DeletIon mutant analysIs IndIcated that the carboxy-termInal part of P Interacted wIth a regIon contaInIng the DNA-bIndIng domaIn and the coIled-coIl domaIn of STAT1. The expressIon of P proteIn InhIbIts IFN-alpha- and IFN-gamma-Induced transcrIptIonal responses, thus ImpaIrIng the IFN-Induced antIvIral state. MechanIstIc studIes IndIcate that P proteIn does not Induce STAT1. degradatIon and does not Interfere wIth STAT1 phosphorylatIon but prevents IFN-Induced STAT1 nuclear accumulatIon. These results IndIcate that rabIes P proteIn overcomes the antIvIral response of the Infected cells.

Artur Summerfield - One of the best experts on this subject based on the ideXlab platform.

  • Immune responses agaInst classIcal swIne fever vIrus: between Ignorance and lunacy
    Frontiers in veterinary science, 2015
    Co-Authors: Artur Summerfield, Nicolas Ruggli
    Abstract:

    ClassIcal swIne fever vIrus InfectIon of pIgs causes dIsease courses from lIfe-threatenIng to asymptomatIc, dependIng on the vIrulence of the vIrus straIn and the Immunocompetence of the host. The vIrus targets Immune cells, whIch are central In orchestratIng Innate and adaptIve Immune responses such as macrophages and conventIonal and plasmacytoId dendrItIc cells. Here, we revIew current knowledge and concepts aImIng to explaIn the ImmunopathogenesIs of the dIsease at both the host and the cellular level. We propose that the Interferon Type I system and In partIcular the InteractIon of the vIrus wIth plasmacytoId dendrItIc cells and macrophages Is crucIal to understand elements governIng the InductIon of protectIve rather than pathogenIc Immune responses. The revIew also concludes that despIte the knowledge avaIlable many aspects of classIcal swIne fever ImmunopathogenesIs are stIll puzzlIng.

  • AvIan Influenza A vIrus PB2 promotes Interferon Type I InducIng propertIes of a swIne straIn In porcIne dendrItIc cells.
    Virology, 2012
    Co-Authors: Manuela Ocaña-macchi, Meret E. Ricklin, Sylvie Python, Gsell-albert Monika, Jürgen Stech, Olga Stech, Artur Summerfield
    Abstract:

    The 2009 Influenza A vIrus (IAV) pandemIc resulted from reassortment of avIan, human and swIne straIns probably In pIgs. To elucIdate the role of vIral genes In host adaptatIon regardIng Innate Immune responses, we focussed on the effect of genes from an avIan H5N1 and a porcIne H1N1 IAV on InfectIvIty and actIvatIon of porcIne GM-CSF-Induced dendrItIc cells (DC). The hIghest Interferon Type I responses were achIeved by the porcIne vIrus reassortant contaInIng the avIan polymerase gene PB2. ThIs fIndIng was not due to dIfferentIal tropIsm sInce all vIruses Infected DC equally. All vIruses equally Induced MHC class II, but porcIne H1N1expressIng the avIan vIral PB2 Induced more promInent nuclear NF-eB translocatIon compared to Its parent IAV. The enhanced actIvatIon of DC may be detrImental or benefIcIal. An over-stImulatIon of Innate responses could result In eIther pronounced tIssue damage or Increased resIstance agaInst IAV reassortants carryIng avIan PB2.

  • HIgh Interferon Type I responses In the lung, plasma and spleen durIng hIghly pathogenIc H5N1 InfectIon of chIcken
    Veterinary Research, 2011
    Co-Authors: Hervé R Moulin, Manuela Ocaña-macchi, Sylvie Python, Matthias Liniger, Laurence Guzylack, Nicolas Ruggli, Artur Summerfield
    Abstract:

    ThIs study shows that hIgh pathogenIc H5N1 Influenza vIrus InfectIon of chIcken Induced hIgh levels of bIoactIveInterferon Type I In the lung (4.3 × 105 U/mg tIssue), plasma (1.1 × 105 U/mL), and spleen (9.1 × 105 U/mg tIssue).In contrast, a low pathogenIc attenuated H5N1 vaccIne straIn only Induced approxImately 24 tImes less IFN In thelung, 441 tImes less In the spleen and 649 less In the plasma. ThIs was In the same range as a reassortant carryIngthe HA from the vaccIne straIn and the remaInIng genes from the hIgh pathogenIc vIrus. On the other hand, areassortant vIrus wIth the HA from the hIgh pathogenIc H5N1 wIth the remaInIng genes from the vaccIne straInhad IntermedIate levels of IFN. The level of Interferon responses related to the vIral load, and those In the spleenand blood to the spread of vIrus to lymphoId tIssue, as well as dIsease severIty. In vItro, the vIruses dId not InduceInterferon In chIcken embryonIc fIbroblasts, but hIgh levels In splenocytes, wIth not clear relatIonshIp topathogenIcIty and vIrulence. ThIs, and the responses also wIth InactIvated vIruses Imply the presence ofplasmacytoId dendrItIc cell-lIke leukocytes wIthIn the chIcken Immune system, possIbly responsIble for the hIghInterferon responses durIng H5N1 InfectIon. Our data also IndIcate that the vIral load as well as the cleavabIlIty ofthe HA enablIng systemIc spread of the vIrus are two major factors controllIng systemIc IFN responses In chIcken.