| Project/Area Number |
13670295
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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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 | Mie University |
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Principal Investigator |
YASUTOMI Yasuhiro Mie University, Faculty of Medicine, Associate Professor, 医学部, 助教授 (90281724)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2002: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2001: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | vaccine / immunology / HCV / Adenovirus vector / hepatitis / アデノウィルスベクター / CTL / 感染モデル |
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| Research Abstract |
Hepatitis C virus (HCV) is one of the major agents of chronic hepatitis and liver disease worldwide. An animal model for HCV infection is required for both vaccine development and for understanding the pathogenesis of HCV infection. Although the chimpanzee is the only known animal model of HCV infection, chimpanzees are difficult to acquire for laboratory animals. In the present study, we assessed the possibility of infection with recombinant adenovirus (rADV-HCV), which is preferential infection to hepatocytes, having cDNA of HCV structural proteins in mice as a novel animal model. Mice were intravascularly inoculated with rADV-HCV. After rADV-HCV inoculation, concentrations of GPT in sera were increased and much higher than control rADV having cDNA of lacZ. These mice inoculated with rADV-HCV showed acute hepatitis in histopathological examination but not control rADV. These high concentrations of GPT in sera were observed for 2 weeks after infection. The HCV-specific CD8+ cytotoxic T lymphocytes (CTLs) were observed after infection with rADV-HCV. The concentrations of GPT in sera were not increased after infection with rADV-HCV, when FK506 or anti-CD8 monoclonal antibody was administered with mice to eliminate these HCV specific CTLs. These studies demonstrated the capacity of murine model induced by inoculation with rADV-HCV to elicit HCV-specific CTL in association with pathogenesis of HCV infection.
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