2016 Fiscal Year Final Research Report
Molecular mechanisms for the acquisition of virulence by bat-borne reoviruses
| Project/Area Number |
26292149
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Veterinary medical science
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| Research Institution | Osaka University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
Kanai Yuta 大阪大学, 微生物病研究所, 助教 (80506501)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | レオウイルス / コウモリ |
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| Outline of Final Research Achievements |
Nelson Bay orthoreoviruses (NBVs) were recently isolated from humans with acute respiratory tract infections, suggesting that NBVs have evolved to propagate in humans. To better understand NBV replication and pathogenesis, we have developed a mouse model of NBV infection that mimics the disease in humans. Furthermore, using reverse genetics, we demonstrated that FAST, p17, and σC proteins encoded by S1 gene segment were not required for viral replication. Our results with mutant viruses demonstrated that fusion activity of FAST was critical for the enhancement of viral replication and that σC was dispensable for cell attachment in several cell lines, including L929 cells but not in A549 cells. Significant attenuation was observed in mice infected with FAST- and σC-deficient viruses compared to those infected with the wild-type, suggesting that FAST and σC play crucial roles in viral pathogenesis, and can provide new insights into the NBV biology.
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| Free Research Field |
ウイルス学
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