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Differential type I IFN-inducing abilities of wild-type versus vaccine strains of measles virus.

Differential type I IFN-inducing abilities of wild-type versus vaccine strains of measles virus. Research Abstract Details 

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  • Differential type I IFN-inducing abilities of wild-type versus vaccine strains of measles virus. Abstract Text:

    masashi shingaiMasashi Shingai,takashi ebiharaTakashi Ebihara,nasim a begumNasim A Begum,atsushi katoAtsushi Kato,toshiki honmaToshiki Honma,kenji matsumotoKenji Matsumoto,hirohisa saitoHirohisa Saito,hisashi oguraHisashi Ogura,misako matsumotoMisako Matsumoto,tsukasa seyaTsukasa Seya,masashi shingaiMasashi Shingai,takashi ebiharaTakashi Ebihara,nasim a begumNasim A Begum,atsushi katoAtsushi Kato,toshiki honmaToshiki Honma,kenji matsumotoKenji Matsumoto,hirohisa saitoHirohisa Saito,hisashi oguraHisashi Ogura,misako matsumotoMisako Matsumoto,tsukasa seyaTsukasa Seya,

    Laboratory adapted and vaccine strains of measles virus (MV) induced type I IFN in infected cells. The wild-type strains in contrast induced it to a far lesser extent. We have investigated the mechanism for this differential type I IFN induction in monocyte-derived dendritic cells infected with representative MV strains. Laboratory adapted strains Nagahata and Edmonston infected monocyte-derived dendritic cells and activated IRF-3 followed by IFN-beta production, while wild-type MS failed to activate IRF-3. The viral IRF-3 activation is induced within 2 h, an early response occurring before protein synthesis. Receptor usage of CD46 or CD150 and nucleocapsid (N) protein variations barely affected the strain-to-strain difference in IFN-inducing abilities. Strikingly, most of the IFN-inducing strains possessed defective interference (DI) RNAs of varying sizes. In addition, an artificially produced DI RNA consisting of stem (the leader and trailer of MV) and loop (the GFP sequence) exhibited potential IFN-inducing ability. In this case, however, cytoplasmic introduction was needed for DI RNA to induce type I IFN in target cells. By gene-silencing analysis, DI RNA activated the RIG-I/MDA5-mitochondria antiviral signaling pathway, but not the TLR3-TICAM-1 pathway. DI RNA-containing strains induced IFN-beta mRNA within 2 h while the same recombinant strains with no DI RNA required >12 h postinfection to attain similar levels of IFN-beta mRNA. Thus, the stem-loop structure, rather than full genome replication or specific internal sequences of the MV genome, is required for an early phase of type I IFN induction by MV in host cells.

    Differential type I IFN-inducing abilities of wild-type versus vaccine strains of measles virus. Publishing Authors By Initials

    m shingaiM Shingai,t ebiharaT Ebihara,na begumNA Begum,a katoA Kato,t honmaT Honma,k matsumotoK Matsumoto,h saitoH Saito,h oguraH Ogura,m matsumotoM Matsumoto,t seyaT Seya,m shingaiM Shingai,t ebiharaT Ebihara,na begumNA Begum,a katoA Kato,t honmaT Honma,k matsumotoK Matsumoto,h saitoH Saito,h oguraH Ogura,m matsumotoM Matsumoto,t seyaT Seya,

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    Differential type I IFN-inducing abilities of wild-type versus vaccine strains of measles virus. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    VOLUME: 179

    Page Numbers: 6123-33

    Journal Abbreviation: J. Immunol.

    ISSN: 0022-1767

    DAY: 1

    MONTH: Nov

    YEAR: 2007

    Differential type I IFN-inducing abilities of wild-type versus vaccine strains of measles virus. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 2985117

    Differential type I IFN-inducing abilities of wild-type versus vaccine strains of measles virus. Keywords Mesh Terms:

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    Chemical & Substance for Abstract: Differential type I IFN-inducing abilities of wild-type versus vaccine strains of measles virus. Information

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    Grant and Affiliation Information for Differential type I IFN-inducing abilities of wild-type versus vaccine strains of measles virus.

    AFFILIATION: Department of Microbiology and Immunology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: J Immunol

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