Strain-to-strain difference of V protein of measles virus affects MDA5-mediated IFN-β-inducing potential
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概要
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Laboratory-adapted and vaccine strains of measles virus (MV) induce type I interferon (IFN) in infected cells to a far greater extent than wild-type strains. We investigated the mechanisms for this differential type I IFN production in cells infected with representative MV strains. The overexpression of the wild-type V protein suppressed melanoma differentiation-associated gene 5 (MDA5)-induced IFN-β promoter activity, while this was not seen in A549 cells expressing CD150 transfected with the V protein of the vaccine strain. The V proteins of the wild-type also suppressed poly I:C-induced IFN regulatory factor 3 (IRF-3) dimerization. The V proteins of the wild-type and vaccine strain did not affect retinoic acid-inducible gene 1 (RIG-I)- or toll-IL-1R homology domain-containing adaptor molecule 1 (TICAM-1)-induced IFN-β promoter activation. We identified an amino acid substitution of the cysteine residue at position 272 (which is conserved among paramyxoviruses) to an arginine residue in the V protein of the vaccine strain. Only the V protein possessing the 272C residue binds to MDA5. The mutation introduced into the wild-type V protein (C272R) was unable to suppress MDA5-induced IRF-3 nuclear translocation and IFN-β promoter activation as seen in the V proteins of the vaccine strain, whereas the mutation introduced in the vaccine strain V protein (R272C) was able to inhibit MDA5-induced IRF-3 and IFN-β promoter activation. The other 6 residues of the vaccine strain V sequence inconsistent with the authentic sequence of the wild-type V protein barely affected the IRF-3 nuclear translocation. These data suggested that the structural difference of vaccine MV V protein hampers MDA5 blockade and acts as a nidus for the spread/amplification of type I IFN induction. Ultimately, measles vaccine strains have two modes of IFN-β-induction for their attenuation: V protein mutation and production of defective interference (DI) RNA.
著者
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Matsumoto Misako
北海道大学 医学研究科免疫学
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Matsumoto M
Department Of Microbiology And Immunology Hokkaido University Graduate School Of Medicine
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Seya Tsukasa
大阪府立成人病センター研究所 免疫学部門
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Seya Tsukasa
北海道大学 医学研究科免疫学
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Seya Tsukasa
Department Of Immunology Osaka Medical Center For Cancer And Cardiovascular Diseases:probrain
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松本 美佐子
Department Of Microbiology And Immunology Hokkaido University Graduate School Of Medicine
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Seto Toshiyuki
Daparment Of Virology
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Matsumoto Masanori
Laboratory Of Immunodynamics Department Of Microbiology And Immunology Osaka University Graduate Sch
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