The diabetogenic capacity of the M-variant of encephalomyocarditis (EMC) virus was markedly diminished after passage in mouse kidney cell cultures. One passage in mice fully restored this capacity. Virus harvested after five passages in either susceptible (SWR/J) or resistant (C57BL/6J) strains of mice was capable of producing diabetes in susceptible SWR/J mice but not in resistant C57BL/6J mice. Resistance was not overcome by inoculating mice with high concentrations of virus. Immunofluorescence studies showed that islets from strains of mice (i.e. CBA, AKR, C57BL/6J, A/J) that did not develop diabetes after infection with EMC virus, nonetheless, contained virus antigens. The percentage of cells in the islets containing virus antigens varied from 3.6% in CBA to 13.5% in A/J. In contrast, 38% of the islet cells in susceptible SWR/J mice contained virus antigens. It is concluded that both the genetic background of the host and the passage history of the virus influence the development of diabetes.


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