| Project/Area Number |
13470064
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Virology
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| Research Institution | Kyushu University |
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Principal Investigator |
YANAGI Yusuke Kyushu University, Faculty of Medicine, Proofessor, 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, Lecturer, 大学院・医学研究院, 講師 (70209823)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥16,400,000 (Direct Cost: ¥16,400,000)
Fiscal Year 2002: ¥7,500,000 (Direct Cost: ¥7,500,000)
Fiscal Year 2001: ¥8,900,000 (Direct Cost: ¥8,900,000)
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| Keywords | measles virus / receptor / SLAM / CD150 / canine distemper virus / rinderpest virus |
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| Research Abstract |
1. By titrating viruses on Vero and Vero/SLAM cells, we show that the great majority of measles viruses in measles patients use SLAM but not CD46 as a cellular receptor, thereby proving that SLAM is the principal receptor for measles virus.
2.We show that although monocytes freshly isolated from peripheral blood mononuclear cells do not express SLAM, its expression is readily induced after stimulation with mitogens or even with measles virus particles. Furthermore, mature dendritic cells, but not immature dendritic cells, also express SLAM. These results indicate that MV infection of monocytes/macrophages and dendritic cells, like that of lymphocytes, is mediated by SLAM.
3. We show that canine distemper virus and rinderpest virus respectively use canine and bovine SLAMs as cellular receptors.
4. By using the recombinant measles virus expressing the green fluorescent protein, we show that wild-type measles virus strains can infect SLAM-negative cells with 2 to 3 logs lower efficiency than it does SLAM-positive cells, indicating the presence of SLAM- and CD46-independent measles virus infection.
5. We show that the interaction of the measles virus H protein with SLAM results in its downregulation from the cell surface, suggesting its involvement in measles virus-induced immunosuppression.
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