| Project/Area Number |
23590534
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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 | Shimane University (2013)
Hokkaido University (2011-2012) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
JINUSHI Masahisa 北海道大学, 遺伝子病制御研究所, 准教授 (40318085)
|
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| Co-Investigator(Renkei-kenkyūsha) |
NANBO Asuka 北海道大学, 医学部, 准教授 (60359487)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | EBウイルス / 病原性 / 腫瘍 / ウイルス / トランスフォーム / 癌 |
|---|
| Research Abstract |
EBV is a ubiquitous human herpes virus with oncogenic activity. Around 10 latent genes are known and many of them play roles for development and maintenance of EBV-associated malignancies. Recently identified BNLF2a gene was expressed at an early lytic infection and contributed evasion of EBV-infected cells from specific CD8+ T cell recognition. Here, we found BNLF2a and novel BNLF2b, of which gene locates 9-bp downstream of BNLF2a gene, were expressed not only at lytic, but at latent infection. Since BNLF2a downregulated surface MHC class I, BNLF2a may contribute establishment of persistently EBV infected B cells in vivo by inducing immune evasion from viral antigen-specific CD8+ T cell recognition. BNLF2b conferred apoptotic resistance to EBV-infected cells, thus supporting proliferation of infected cells. Suggesting that both BNLF2a and BNLF2b contribute to development of EBV-associated malignancies through proliferation of EBV-infected cells.
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