| Project/Area Number |
08457265
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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 |
内分泌・代謝学
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| Research Institution | Osaka University |
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Principal Investigator |
NAKAJIMA Hiromu Osaka University, Faculty of Medicine, Assistant Professor, 医学部, 助手 (50252680)
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| Co-Investigator(Kenkyū-buntansha) |
ASAKAWA Hideki Osaka University, Faculty of Medicine, Assistant Professor, 医学部, 助手 (60283785)
MIYAGAWA Jun-ichiro Osaka University, Faculty of Medicine, Assistant Professor, 医学部, 助手 (00127721)
NAMBA Mitsuyoshi Osaka University, Faculty of Medicine, Assistant Professor, 医学部, 助手 (00183533)
HANAFUSA Toshiaki Osaka University, Faculty of Medicine, Lecturer, 医学部, 講師 (60164886)
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| Project Period (FY) |
1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥5,000,000 (Direct Cost: ¥5,000,000)
Fiscal Year 1996: ¥5,000,000 (Direct Cost: ¥5,000,000)
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| Keywords | type 1 diabetes mellitus / retrovirus / positional cloning / disease susceptible gene / viral infection / pancreas beta-cell destruction / NOD mouse / gene delivery method / 組織適合抗原遺伝子 |
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| Research Abstract |
The non-obese diabetic (NOD) mouse develop type I diabetes mellitus characterized by a massive lymphocytic infiltration into the pancreatic islets. A viral role has been suggested in the pathogenesis of this type of diabetes mellitus. We report here the cloning of retrovirus cDNA whose expression was considered to be specific to the pancreas of the NOD mouse. The provirus differs in sequence from all other published type C retrovirsues. The virus has a relatively well conserved gag region, and a truncated pol region with a large deletion. Almost all env region were deleted, and a trace of the sequence motif was included 3'to the pol region. These structural features are characteristic of replication defective viruses. Viral mRNA expression level was highest in 4-week-old NOD mice. The onset of insulitis also occurs from 4 weeks of age in the NOD mouse, thus suggesting a role for the virus in the pathogenesis of diabetes in this animal model.
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