Role of the regulation of B cell protein-tyrosine kinase by hepatitis C virus

2015 Fiscal Year Final Research Report

• Project/Area Number: 25460383
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Pathological medical chemistry
• Research Institution: University of Fukui
• Principal Investigator: SADA Kiyonao 福井大学, 医学部, 教授 (10273765)
• Co-Investigator(Kenkyū-buntansha): CHIHARA Kazuyasu 福井大学, 医学部, 准教授 (00314948) ; TAKEUCHI Kenji 福井大学, 医学部, 助教(学内講師) (40236419) ; YAMAUCHI Shota 福井大学, 医学部, 特命助教 (00728941)
• Co-Investigator(Renkei-kenkyūsha): HOTTA Hak 神戸大学, 保健学研究科, 教授 (40116249)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: C型肝炎ウイルス / チロシンキナーゼ

Outline of Final Research Achievements

Hepatitis C virus (HCV) infects B lymphocytes and induces B cell lymphoma, in addition to chronic hepatitis and hepatocellular carcinoma. However, molecular mechanism for the pathogenesis of HCV infection-mediated disorders remains unclear. In this study, we investigated the role of protein-tyrosine kinases on HCV lifecycle, because HCV interacts with protein-tyrosine kinases in B cells. As a result, we found that HCV particle assembly involves phosphorylation of NS5A (non-structural protein of HCV) by the c-Abl protein-tyrosine kinase.
In parallel with this study, we investigated the molecular mechanism of infection immunity. We identified the novel mast cell anti-fungal immunity through Dectin-1 and Syk, and novel regulatory mechanism of Syk substrate 3BP2 (c-Abl SH3 domain-binding protein-2) in B cells.

Free Research Field

ウイルス学、生化学