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Studies on mechanism of infectious bursal disease virus infection to the target cells and molecular analysis of cellular receptor for the virus binding.

传染性法氏囊病病毒感染靶细胞的机制研究及病毒结合细胞受体的分子分析。

基本信息

批准号：
12660269
负责人：
YAMAGUCHI Tsuyoshi
金额：
$ 2.3万
依托单位：
Gifu University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2000
资助国家：
日本
起止时间：
2000 至 2002
项目状态：
已结题

项目摘要

To clarify the mechanism of infectious bursal disease virus (IBDV) infection to the target cells and interaction between the virus and the cells, some analyses on cellular receptor for the virus binding and viral protein interacts with the cellular molecule were made.1. Identification of cellular molecules which bind to IBDV particle.It is defined that the cellular molecules of cell membrane proteins, 70, 82 and 110 kDa, are specifically bind to IBDV particle.2. Isolation of monoclonal antibodies which recognize receptor molecule of IBDV.Monoclonal antibodies which recognize 110 kDa membrane protein of LSCC-BK3 cell specifically inhibit the binding of IBDV to the cell. This finding strongly suggests that the 110 kDa molecule is cellular receptor for the virus infection.3. Production of anti-idiotypic antibody specific for an IBDV-neutralizing monoclonal antibody.Anti-idiotypic antibody specific for an IBDV-neutralizing monoclonal antibody, GI-11 which recognizes VP2 hypervariable domain, does not interfere with the virus infection. This finding indicates that hydrophilic amino acid sequences at both ends of the domain recognized by GI-11 is not essential for the virus infection or binding to the target cells.4. Studied on cytotoxicity of IBDV to the target cells.Viable cell number is significantly reduced after the infection of classical strains of IBDV in comparison with the highly virulent strains infected cells. In addition, there were no differences in the virus titer and the rate of virus antigen positive cells between the classical and highly virulent strain infected cells. These findings indicate that classical IBDV strain is more cytotoxic in comparison with the highly virulent strains.

为阐明传染性法氏囊病病毒（IBDV）感染靶细胞的机制及病毒与靶细胞的相互作用，对病毒结合的细胞受体及病毒蛋白与细胞分子的相互作用进行了分析.与IBDV病毒颗粒结合的细胞分子的鉴定：确定与IBDV病毒颗粒特异性结合的细胞膜蛋白分子为70、82和110 kDa.识别IBDV受体分子的单克隆抗体的分离识别LSCC-BK 3细胞110 kDa膜蛋白的单克隆抗体特异性地抑制IBDV与细胞的结合。这一发现有力地表明，110 kDa分子是病毒感染的细胞受体。特异性针对IBDV中和性单克隆抗体的抗独特型抗体的制备特异性针对IBDV中和性单克隆抗体GI-11的抗独特型抗体识别VP 2高变区，不干扰病毒感染。这一发现表明GI-11识别的结构域两端的亲水性氨基酸序列对于病毒感染或结合靶细胞不是必需的.研究了传染性法氏囊病病毒（IBDV）对靶细胞的细胞毒作用，发现IBDV经典毒株感染细胞后，活细胞数较强毒株感染细胞后明显减少。此外，经典毒株和强毒株感染细胞的病毒滴度和病毒抗原阳性细胞率无差异。这些结果表明，经典毒株比强毒株具有更强的细胞毒性。