Analysis for molecular mechanism of hepatitis C virus(HCV)-induced protein associated with persistent HCV infection
Project/Area Number |
24659371
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Multi-year Fund |
Research Field |
Gastroenterology
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Research Institution | Kagoshima University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
宇都 浩文 鹿児島大学, 大学院・医歯学総合研究科, 講師 (20347058)
|
Research Collaborator |
馬渡 誠一 , 大学院生
|
Project Period (FY) |
2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
|
Keywords | 肝臓学 / HCV / セリンプロテアーゼ / 補体C4 / 断片化 |
Research Abstract |
The mechanisms underlying the persistence of Hepatitis C virus(HCV) infection are hypothesized to involve viral proteins abrogating the host immune response. Here, we report that HCV NS3/4A protease is associated with production of the C4 fragment and that this action affects the host immune response. In vitro, HCV NS3/4A protease showed concentration-dependent cleavage of C4 and a HCV NS3/4A protease inhibitor inhibited this cleavage. Functionally, cleavage of C4by HCV NS3/4A protease inhibited the classical pathway and this inhibition was also abrogated by a HCV NS3/4A protease inhibitor. Our results indicate that HCV NS3/4A protease inhibits complement activation through cleavage of C4, and that C4 cleavage by HCV NS3/4A protease should be one of the mechanisms underlying persistent HCV infection.
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Report
(2 results)
Research Products
(4 results)
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[Presentation] Hepatitis C virus NS3/4A protease inhibits complement activation through cleavage of complement component C42012
Author(s)
Mawatari S, Uto H, Sato Y, Kumagai K, Oda K, Tabu K, Tamai T, Moriuchi A, Oketani M, Ido A, Suzuki T, Tsubouchi H
Organizer
The 63th Annual Meeting of the American Association for the Study of Liver Diseases
Place of Presentation
Boston, MA, USA
Related Report
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