Isolation of cell surface molecules responsible for binding with Hepatitis B virus
| Project/Area Number |
24590563
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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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 |
Suzuki Ryosuke 国立感染症研究所, その他部局等, 研究員 (50342902)
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| Co-Investigator(Kenkyū-buntansha) |
KURODA Shun'ichi 大阪大学, 産業科学研究所, 教授 (60263406)
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| Research Collaborator |
Matsuda Mami 国立感染症研究所, ウイルス第二部, 協力研究員
Saga Ryohei 国立感染症研究所, ウイルス第二部, 研究生
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| Project Period (FY) |
2012-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | B型肝炎ウイルス / 細胞表面蛋白質 |
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| Outline of Final Research Achievements |
Cell surface molecules responsible for binding with Hepatitis B virus (HBV) were examined using yeast-derived recombinant HBV particles. The viral particles are composed of L protein, which is indispensable for viral entry. Several human-derived cell lines were examined for binding with the particle. Using the Stable Isotope Labeling by Amino Acids in Cell Culture (SILAC) method, we identified candidates of cell surface molecules for interaction with the viral particle. Following by siRNA screening, Scavenger receptor class B member 1 (SRB1) was identified as a binding molecule for the viral particles. However, knockdown or knockout of SRB1 in sodium taurocholate cotransporting polypeptide (NTCP)-expressing HepG2 had no effect on HBV infection. These results strongly suggest that SRB1 is not associated with HBV entry. Further research is needed, but with a different approach.
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Report
(5 results)
Research Products
(12 results)
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[Journal Article] Interleukin-1 and tumor necrosis factor-α trigger restriction of hepatitis B virus infection via a cytidine deaminase activation-induced cytidine deaminase (AID)2013
Author(s)
Watashi K, Liang G, Iwamoto M, Marusawa H, Uchida N, Daito T, Kitamura K, Muramatsu M, Ohashi H, Kiyohara T, Suzuki R, Li J, Tong S, Tanaka Y, Murata K, Aizaki H, Wakita T
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Journal Title
J Biol Chem
Volume: 288
Issue: 44
Pages: 31715-31727
DOI
NAID
Related Report
Peer Reviewed
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