| Project/Area Number |
03670445
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Toyama Medical & Pharmaceutical University |
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Principal Investigator |
KISHIMOTO Chiharu Toyama Med.& Pharm.Univ., 2nd Dept.of Intern. Med., Instructor, 医学部, 助手 (70169845)
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| Co-Investigator(Kenkyū-buntansha) |
KUROKAWA Masahiko Toyama Med.& Pharm.Univ., Dept.of Virology, Instructor, 医学部, 助手 (80186527)
OCHIAI Hiroshi Toyama Med.& Pharm.Univ., Dept.of Virology, Associate Professor, 医学部, 助教授 (30018692)
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| Project Period (FY) |
1991 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1993: ¥200,000 (Direct Cost: ¥200,000)
Fiscal Year 1992: ¥200,000 (Direct Cost: ¥200,000)
Fiscal Year 1991: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Viral myocarditis / Dilated cardiomyopathy / Antibody / T-lymphocyte / Reinfection / Superposed infection / Coxsackievirus B3 |
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| Research Abstract |
Fc receptor (FcR)-mediated coxsackievirus B3 (CB3) infection in vitro and in vivo was investigated. When P388D1 cells (a murine macrophage-like cell line) were infected with CB3 exposed previously to various concentrations of anti-CB3 rabbit immunoglobulin G (Igg) or its Fab fragment, enhanced infection of CB3 was observed at a subneutralizing concentration of IgG, but not of Fab fragment. In addition, we confirmed the existence of this infectious pathway in vivo. C_3H/He mice with various levels of immunity by preinoculation of amyocarditic CB3 were reinoculated with myocarditic CB3. The severity of myocarditis and myocardial Cb3 titers were markedly enhanced in the mice with a low level of immunity compared to those with high or no immunity. Therefore, the insufficient immunity may not always provide a benign or protective influence. This immunological response facilitates the reinfection possibly inducing chronic active myocarditis.
In addition, enterovirus-primed memory T cells would react similarly in vivo to a secondary inoculation with any cardiotropic enterovirus that shares an epitope(s) with the primary challenge virus. Thus, T cell-mediated immune responses to conserved antigenic epitopes among the enteroviruses was involved in the exacerbation of myocardial inflammatory disease during a second enterovirus infection. The secondary infection model may more accurately mirror virus-induced myocarditis in the human population because the majority of adults have exposed t several enteroviruses before induction of disease.
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