| Project/Area Number |
26860307
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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 |
Virology
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| Research Institution | National Institute of Infectious Diseases |
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Principal Investigator |
SUZUKI Tadaki 国立感染症研究所, 感染病理部, 室長 (30527180)
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| Research Collaborator |
TAKAHASHI Kenta 国立感染症研究所, 感染病理部, 主任研究官
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ヴァイロポリン / ポリオーマウイルス / JCウイルス / 内因性ウイルス感染制御因子 / JCPyV / 進行性多巣性白質脳症 / JCV / 細胞障害 |
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| Outline of Final Research Achievements |
Viroporins are small and hydrophobic viral proteins that assemble into ion-channel like structures on host cell membranes. Expression of viroporins in viral replicaiton can increase the infected cell’s membrane permeability and the secretion of progeny virions. JC virus (JCV), belongs to polyomavirus family, is the causative agent of progressive multifocal leukoenchephalopathy (PML). Recently we have demonstrated that JCV Agno acts as a JCV viroporin. Furthermore, we also demonstrate that an interaction of Agno with a host cellular protein modulates the viroporin activity of Agno. These findings indicate the host cellular protein can detect JCV infection and play a role in restriction of viral replication. These proteins, which are described as intrinsic antiviral factors, interact directly with viral components and suppress viral replication directly. In this study, we explored intrinsic antiviral factors against polyomavirus viroporins.
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