| Project/Area Number |
21790443
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Virology
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| Research Institution | Osaka University |
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Principal Investigator |
TANI Hideki Osaka University, 微生物病研究所, 特任助教 (20397706)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 分子 / C型肝炎ウイルス(HCV) / シュードタイプウイルス / 組換えウイルス / 水疱性口内炎ウイルス / レセプター / テトラシステインタグ |
|---|
| Research Abstract |
The receptors of HCV have been characterized, yet the entry pathways of the HCV into target cells are incompletely defined. As a surrogate virus system, pseudotype viruses transiently bearing HCV envelope proteins based on the vesicular stomatitis virus (VSV) and retrovirus or cell cultured HCV (HCVcc) have been developed. Here, we have tried to develop a fluorescence-labeled pseudotype VSV or recombinant VSV for a visualized investigation of the entry mechanisms. Furthermore, to characterize the mechanisms by which HCV infection activates downstream signaling pathways, we utilized a pseudotype vesicular stomatitis virus possessing HCV envelope proteins (HCVpv) and JFH-1 virus in combination with pharmacological inhibitors. We reported that HCV utilizes the phospholipase C (PLC) / protein kinase C (PKC)-dependent signaling for the entry. Inhibition of actin rearrangement by actin-depolymerizing reagents markedly diminishes HCVpv infection. Overall, these results indicate that the activation of PLC and PKC-dependent pathway is required for the entry of HCV and is involved in setting the actin rearrangement for the endocytosis of the virus.
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