Reverse genetics system for Ibaraki virus reveals the mechanisms of double-stranded virus replication
| Project/Area Number |
15K21152
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Veterinary medical science
Virology
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| Research Institution | Kobe University |
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Principal Investigator |
MATSUO EIKO 神戸大学, 農学研究科, 助教 (40620878)
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| Research Collaborator |
ROY POLLY London School of Hygiene & Tropical Medicine, 教授
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 二本鎖RNAウイルス / タンパク質発現抑制 / 標識IBAV / FACS解析 |
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| Outline of Final Research Achievements |
Ibaraki virus (IBAV) is a member of the epizootic hemorrhagic disease virus serogroup, which belongs to the Orbivirus genus of the Reoviridae family. Although EHDV infection in cattle is subclinical in most cases, EHDV, including IBAV, is still an ongoing threat to livestock in the world. Recently we developed reverse genetics system (RG) for IBAV, to clarify the molecular mechanism of orbivirus replication. In addition, we found several cell lines, in which, the replication of IBAV was suppressed. Here, we newly developed plasmid-based RG for IBAV to produce fluorescent-labeled IBAV (FL-IBAV). Using FL-IBAV, IBAV binding to host-cells was visualized and the binding ability of IBAV was quantified. In addition, together with previous studies, we demonstrated that the suppression of IBAV replication in the several cell lines was likely to occur after transcription step, not entry step. Further, we tried to reveal the involvement of autophagy in the enhancement of IBAV replication.
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Report
(4 results)
Research Products
(23 results)
