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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.

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。
批准号:
12660269
负责人:
YAMAGUCHI Tsuyoshi
金额:
$2.3万
依托单位:
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
项目状态:
已结题
起止时间:
2000 至 2002

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中文摘要
翻译
为了阐明传染性法氏囊病病毒(IBDV)感染靶细胞的机制以及病毒与细胞的相互作用,本文对病毒结合的细胞受体以及病毒蛋白与细胞分子的相互作用进行了分析。结合IBDV颗粒的细胞分子鉴定。定义了70、82和110 kDa的细胞膜蛋白的细胞分子特异性结合IBDV颗粒。识别IBDV受体分子的单克隆抗体的分离。识别LSCC-BK3细胞110 kDa膜蛋白的单克隆抗体特异性抑制IBDV与细胞的结合。这一发现强烈提示110 kDa分子是病毒感染的细胞受体。ibdv中和单克隆抗体特异性抗独特型抗体的产生。ibdv中和单克隆抗体特异性抗独特型抗体GI-11识别VP2高变结构域,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与靶细胞结合不是必需的。研究了IBDV对靶细胞的细胞毒性。与高毒力菌株感染的细胞相比,经典菌株感染后的活细胞数量显著减少。此外,在病毒滴度和病毒抗原阳性细胞率在经典和高毒力株感染细胞之间没有差异。这些结果表明,与高毒力菌株相比,经典IBDV菌株具有更强的细胞毒性。
英文摘要
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.
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会议论文
Yamaguchi, T., Igusa, A., Setiyono, A., Fukushi, H., Hirai, K.: "Anti-idiotyptc antibody specific for an infectious bursal disease virus-neutralizing monoclonal antibody does not interfere with the virus infection"Archives of Virology. 147. 2017-2033 (200
Yamaguchi, T.、Igusa, A.、Setiyono, A.、Fukushi, H.、Hirai, K.:“针对传染性法氏囊病病毒中和单克隆抗体特异性的抗独特型抗体不会干扰病毒感染”档案
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通讯作者:
Setiyono, A., Yamaguchi, T., Ogawa, M., Fukushi, H., Hirai, K.: "Isolation of monoclonal antibodies that inhibit the binding of infectious bursal disease virus to LSCC-BK3 cells"Journal of Veterinary Medical Science. 63. 215-218 (2001)
Setiyono, A.、Yamaguchi, T.、Okawa, M.、Fukushi, H.、Hirai, K.:“抑制传染性法氏囊病病毒与 LSCC-BK3 细胞结合的单克隆抗体的分离”兽医医学杂志
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通讯作者:
Yamaguchi, T., Igusa, A., Setiyono, A., Fukushi, H., Hirai, K.: "Anti-idiotypic antibody specific for an infectious bursal disease virus-neutralizing monoclonal antibody does not interfere with the virus infection"Archives of Virology. 147. 2017-2023 (200
Yamaguchi, T.、Igusa, A.、Setiyono, A.、Fukushi, H.、Hirai, K.:“针对传染性法氏囊病病毒中和单克隆抗体的特异性抗独特型抗体不会干扰病毒感染”档案
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通讯作者:
Agus,Setiyono: "Isolation of monoclonal antibodies that inhibit the binding of infectious bursal disease virus to LSCC-BK3 cells."J.Vet.Med.Sci.. 63. 215-218 (2001)
Agus, Setiyono:“抑制传染性法氏囊病病毒与 LSCC-BK3 细胞结合的单克隆抗体的分离。”J.Vet.Med.Sci.. 63. 215-218 (2001)
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