| Project/Area Number |
11470077
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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 | National Institute of Infections Diseases |
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Principal Investigator |
KATO Atsushi National Institute of Infections Diseases, Chief, ウイルス製剤部, 室長 (40152699)
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| Co-Investigator(Kenkyū-buntansha) |
SAKAI Yuko T Institute of Medical Science, Tokyo University Research associate, 医科学研究所, 教務職員 (40178538)
NAGAI Yoshiyuki Toyama Institute of Health, Director, センター長 (20022874)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥6,900,000 (Direct Cost: ¥6,900,000)
Fiscal Year 2001: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 2000: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1999: ¥2,800,000 (Direct Cost: ¥2,800,000)
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| Keywords | Sendai virus / paramyxovirus / reverse genetics / C protein / RNA synthesis / Interferon / Innate immunity / 終結配列 / リードスルー / 粒子形成 |
|---|
| Research Abstract |
An ORF overlapping the ammo-terminal portion of the Sendai virus (SeV) P ORF in the +1 frame produces a nested set of carboxy-coterminal proteins, C,' C, Yl and Y2, which are referred to collectively as the C proteins. The C proteins are an extremely versatile triple-role player ; they counteract the anti-viral action of interferons (IFNs), inhibit viral RNA synthesis and are involved in virus assembly. Here, we established HeLa cell lines stably expressing the C, Y1 and Y2 proteins individually and examined the capacity of these cells to circumvent the anti-viral action of IFNs and to inhibit the viral transcription. The data obtained clearly indicated that the smallest Y2 protein was as active as the C and Y1 proteins in both counteracting the anti-viral action of IFNs and inhibiting viral transcription.
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