| Project/Area Number |
10180101
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| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas (A)
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | TOHOKU UNIVERSITY (2000-2001)
The University of Tokyo (1998-1999) |
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Principal Investigator |
KOYANAGI Yoshio (2000-2001) Tohoku University, Graduate School of Medicine, Professor, 医学系研究科, 教授 (80215417)
永井 美之 (1998-1999) 東京大学, 医科学研究所, 教授 (20022874)
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| Co-Investigator(Kenkyū-buntansha) |
MASUDA Takao Tokyo Medical and Dental University, Medical Research Division, Associate Professor, 医歯学総合研究科, 助教授 (80219336)
OKAMOTO Takashi Nagoya City University, Faculty of Medicine, Professor, 医学部, 教授 (40146600)
SHIODA Tatsuo Osaka University, Research Institute for Microbial Diseases, Professor, 微生物病研究所, 教授 (00187329)
SHIDA Hisatoshi Hokkaido University, Institute for Genetic Medicine, Professor, 遺伝子病制御研究所, 教授 (00144395)
足立 昭夫 徳島大学, 医学部, 教授 (90127043)
高橋 秀宗 国立感染症研究所, 主任研究員 (70260271)
生田 和良 大阪大学, 微生物病研究所, 教授 (60127181)
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| Project Period (FY) |
1998 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥185,100,000 (Direct Cost: ¥185,100,000)
Fiscal Year 2001: ¥45,100,000 (Direct Cost: ¥45,100,000)
Fiscal Year 2000: ¥42,800,000 (Direct Cost: ¥42,800,000)
Fiscal Year 1999: ¥45,000,000 (Direct Cost: ¥45,000,000)
Fiscal Year 1998: ¥52,200,000 (Direct Cost: ¥52,200,000)
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| Keywords | HIV-1 / AIDS / CD4(+) T cell / NF-kappaB / Chemokine receptor / Retrovirus / Integration / Nuclear export / ゲノム / TAT / インテグレース / REV / 核内因子 / HIV-1 / gp41 / Nef / 阻害剤 / RANTES / サル細胞 / SIV / SDFA / CD26 / 糖鎖 / 逆転写 / アクセサリー蛋白 / サブタイプEゲノム |
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| Research Abstract |
Koyanagi reported that TRAIL but not FasL was involved in the apoptotic death of CD4(+) T cells in infected individuals using SCID-PBL mouse system. Furthermore, they showed that TRAIL was also involved in the neuronal cell death in a murine model of HIV central nervous system infection. Shioda identified a deletion mutation in the CCR5 gene specifically seen in Asian population and showed that this mutation affected the surface trafficking of CCR5, resulting in the low sensitivity to HIV-1 infection in the affected individuals. Okamoto identified the host factors essential for viral transcription. One was AES/TLE, as a co-repressor of NF-kappaB p65. Another was FUS/TLS, as a co-activator of NF-kappaB. Masuda found a novel nuclear import signal located in HIV-1 integrase. Shida reported that CRAM1 is necessary for the oligomerization of Rev protein and that human CRAM1 also functioned even in murine cells.
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