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

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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.