Project/Area Number |
14370098
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Virology
|
Research Institution | HOKKAIDO UNIVERSITY |
Principal Investigator |
SHIDA Hisatoshi Hokkaido.Univ., Institute for Genetic Medicine, Professor, 遺伝子病制御研究所, 教授 (00144395)
|
Co-Investigator(Kenkyū-buntansha) |
KIDOKORO Minoru Institute for Infectious Disease, Department of Virology III, Principal Investigator, 主任研究官 (00370958)
HAKATA Yoshiyuki Hokkaido Univ., Institute for Genetic Medicine, Assistant professor, 遺伝子病制御研究所, 助手 (30344500)
YASUDA Jiro Nat.Res.Inst.of Police Sci.JAPAN, Department of First Forensic Science, Chief, 室長 (10282518)
山田 雅巳 北海道大学, 遺伝子病制御研究所, 助手 (10322851)
|
Project Period (FY) |
2002 – 2003
|
Project Status |
Completed (Fiscal Year 2003)
|
Budget Amount *help |
¥13,400,000 (Direct Cost: ¥13,400,000)
Fiscal Year 2003: ¥4,800,000 (Direct Cost: ¥4,800,000)
Fiscal Year 2002: ¥8,600,000 (Direct Cost: ¥8,600,000)
|
Keywords | HTLV-1 / Rex / CRM1 / rat / Infection animal model |
Research Abstract |
Human T cell leukemia virus type1 (HTLV-1) replicates poorly in rats owing to a low activity of Rex in rat cells. Rat autholog of human CRM 1, a cofactor of Rex, is found to be responsible for the poor activity of Rex, because it does not support the Rex multimerization, which is essential for viral RNA export. In this Project, we intended to demonstrate that rat CRM1 is a major block against HTLV-1replication and expression of human CRM1 in rat cells is sufficient to recover viral protein synthesis. Finally we aimed to produce a transgenic rat expressing human CRM1. Then we have gotten the following results. 1, The human CRM1expressing rat cell lines were successfully established. 2, In the parental rat cells, Rex activity was at undetectable level, while in the human CRM1-transduced rat cells, the Rex activity was significantly enhanced to the level similar to the human cells. 3, Furthermore, the expression of human CRMI efficiently recovered the ability of HTLV-1 to produce viron proteins. 4, We could successfully produce a transgenic rat expressing human CRM1.
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