ABSTRACT
D variant of encephalomyocarditis (EMC-D) virus causes diabetes in susceptible mice by direct infection and cytolysis of pancreatic beta cells. cDNA covering the major outer capsid protein (VP1) of EMC-D virus was cloned into Mycobacterium bovis bacillus Calmette-Guerin (BCG). None of the SJL/J male mice, immunized with live recombinant BCG-VP1, became diabetic when challenged with highly diabetogenic EMC-D virus. But the control mice inoculated with normal BCG or rBCG transformed with vector alone developed diabetes in the same challenge. VP1-specific antibodies including neutralizing antibodies were markedly increased as time went on and reached to the maximum titer at week 10 after a single immunization. The plateau of the titer lasted longer than following 4 weeks. Guinea pigs immunized with the live rBCG-VP1 showed strong delayed type hypersensitivity (DTH) to the VP1of EMC-D virus. It means that the live rBCG-VP1 elicit efficient humoral and cell-mediated imrnune responses against EMC-D virus, resulting in prevention of virus-induced diabetes in susceptible mice.