| Project/Area Number |
02670193
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Virology
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| Research Institution | Kanazawa University, Cancer Research Institute |
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Principal Investigator |
SATO Hiroshi Kanazawa University Cancer Research Institute Research Associate, がん研究所, 助手 (00115239)
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| Co-Investigator(Kenkyū-buntansha) |
滝元 徹 金沢大学, 医学部, 講師 (60143905)
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| Project Period (FY) |
1990 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1991: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1990: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | EV viurs / Nasopharyngeal carcinoma / Cell fusion / 上皮咽頭癌 / 末端反複配列 |
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| Research Abstract |
NPC-KT cl. S61, a subclone derived from an epithelial-nasopharyngeal carcinoma hybrid cell line NPC-KT, showed extensive Epstein-Barr virus (EBV) production and cytophapthic changes characteristic of herpes virus replication, including formation of multi-nucleated giant cells and inclusion bodies, when EBV replicative cycle was induced by 5-iodo-2'-deoxyuridine. Syncytia formation of cl. S61 sells was inhibited by 2-deoxyglucose and Acyclovir, inhibitors of glycosylation and EBV DNA polymerase, respectively, with a concomitant decrease in the number of cells expressing EBV growth-associated antigens to the level of parental NPC-KT cells, which did not form syncytia during virus synthesis. However, the frequency of virus antigen expression in NPC-KT cells was not significantly affected. These results suggest that the EBV replicative cycle spreads via cell fusion in cl. S61 cells. It was also demonstrated by in situ autoradiography that cl. S61 cells producing virus fused to not only EBV receptor/CR2 positive Raji and BJAB cells but also to receptor negative Jurkat cells. The possible mechanism of entry of EBV into cells devoid of virus recptor by cell fusion is discussed.
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