2004 Fiscal Year Final Research Report Summary
INTERACTION BETWEEN MEASLES VIRUS AND INNATE IMMUNITY
Project/Area Number |
15390151
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Virology
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Research Institution | KYUSHU UNIVERSITY |
Principal Investigator |
YANAGI Yusuke Kyushu University, Faculty of Medicine, Professor, 大学院・医学研究院, 教授 (40182365)
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Co-Investigator(Kenkyū-buntansha) |
MINAGAWA Hiroko Kyushu University, Faculty of Medicine, Associate Professor, 大学院・医学研究院, 助教授 (70209823)
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Project Period (FY) |
2003 – 2004
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Keywords | measles virus / interferon |
Research Abstract |
To replicate efficiently in the hosts, viruses have evolved various countermeasures to the Interferon (IFN) response. The V protein of measles virus (MV) has been shown to block IFN-alpha/beta signaling. Here, the wild-type IC-B strain of MV was shown to grow comparably in the presence and absence of IFN-alpha, whereas replication of the Edmonston tag strain recovered from cloned DNA was strongly suppressed in its presence. The V protein of the IC-B strain, but not the Edmonston tag strain, blocked IFN-alpha signaling. The V protein of the Edmonston strain from the ATCC also inhibited IFN-alpha signaling. There were three amino acid differences between the V proteins of the Edmonston ATCC and tag strains, and substitutions of both residues at positions 110 and 272 were required for the Edmonston ATCC V protein to lose IFN-antagonist activity. The P protein of the IC-B strain, which shares the N-terminal 231 as residues with the V protein, also inhibited IFN-alpha signaling. Indeed, fragments comprising only those 231 residues of the IC-B and Edmonston ATCC V proteins, but not the Edmonston tag V protein, were able to block IFN-alpha signaling. However, the N-terminal region of the Edmonston tag V protein, when attached to the C-terminal region of the Edmonston ATCC V protein, inhibited IFN-alpha signaling. Taken together, our results indicate that both the N- and C-terminal regions contribute to the IFN-antagonist activity of the MV V protein.
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Research Products
(12 results)
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[Journal Article] Genetic evidence linking SAP, the X-linked lymphoproliferative gene product, to Src-related kinase FynT in TH2 cytokine regulation.2004
Author(s)
Davidson D, Shi X, Zhang S, Wang H, Nemer M, Ono N, Ohno S, Yanagi Y, Veillette A.
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Journal Title
Immunity 21
Pages: 707-717
Description
「研究成果報告書概要(欧文)」より
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