| Project/Area Number |
07457589
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Hokkaido University |
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Principal Investigator |
TAKADA Kenzo Hokkaido University School of Medicine, Cancer Institute, Department of Virology, Professor, 医学部, 教授 (30133721)
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| Co-Investigator(Kenkyū-buntansha) |
SUGIURA Makoto Hokkaido University School of Medicine, Cancer Institute, Department of Virology, 医学部, 助手 (20241317)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1996: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Epstein-Barr virus / latent infection / activation / anti-immunoglobulin antibody / promoter / 転写制御 |
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| Research Abstract |
This study aimed to identify factors regulating the expression of the BZLF1 gene which acts as the switch for shift from Epstein-Barr virus (EBV) latent infection to virus replicative cycle. Burkitt's lymphoma-derived Akata cells have a very unique property that cells are in a latent state of EBV infection and shift to virus replicative cycle upon treatment of cells by anti-immunoglobulin antibodies (anti-Ig). Recently, we have isolated EBV-negative subclones from parental Akata cells. By using EBV-negative Akata cells, we searched for cellular genes involved in virus induction from latent infection.
Nuclear extract was isolated from anti-Ig-treated and -untreated cells and analyzed by a gel shift assay with probes specific for 3 BZLF1 promoter regions that had been shown to be important for BZLF1 expression (Shimizu et al., J.Virol.67 : 3240-3245,1993). We could see many bands, however the competition experiments revealed that none of them was specific. Further study with different conditions may allow to identify specifc bands.
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