| Project/Area Number |
18590462
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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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 | National Institute of Infectious Diseases |
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Principal Investigator |
MURAYAMA Asako National Institute of Infectious Diseases, Department of Virology II, Scientist (40415534)
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| Co-Investigator(Kenkyū-buntansha) |
WAKITA Takaji National Institute of Infectious Diseases, Department of Virology II, Director (40280789)
DATE Tomoko National Institute of Infectious Diseases, Department of Virology II, Scientist (40392360)
MORIKAWA Kenichi National Institute of Infectious Diseases, Department of Virology II, Scientist (60384377)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥4,010,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥510,000)
Fiscal Year 2007: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | HCV / Virus / Virus replication / adaptation / Infection / ウイルスゲノム複製 / 変異 / 慢性肝炎 / 肝臓癌 |
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| Research Abstract |
We have established HCV culture system using JFH-1 strain isolated from a fulminant hepatitis patient. This system enabled us to analyze HCV life cycles in detail. In this research project, we have analyzed how HCV adapted in cultured cells and organisms. We have also tried to determine which virus components involved in HCV adaptation.
HCV adaptation in cultured cells: we transfected in vitro-synthesized HCV RNA into Huh7 cells and collected infectious HCV particles. HCV infection sometimes causes plaque formation. We collected plaque forming HCVs, and infected to naive Huh7 cells. Isolated virus subclones from individual plaque showed greater replication efficiency and cytopathogenicity than parental virus. We analyzed the sequence of this HCV and found several nucleotide mutations with amino acid substitution in NS5B coding region. These mutations may be involved in plaque forming ability and virus genome replication.
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