The diabetogenic variant of encephalomyocarditis virus (EMC-D) induces a diabeteslike syndrome in certain strains of mice. A study was done to determine if virus-induced diabetes could be prevented by interferon (IFN). It was found that the production of diabetes by EMC-D was blocked by either IF", or a variety of IFN-inducers in SWR/J, but not ICR Swiss mice. The replication of EMC-D in cell culture was inhibited by IFN,. It is concluded that the response of pancreatic beta cells to the protective effect of IFN, is probably under genetic control.

The diabetogenic strain of encephalomyocarditis virus (D virus) was propagated in several continuous cell lines. Each virus stock was tested for its ability to produce diabetes in mice and induce L-cell interferon (IFN-beta). The effect of insulin on virus replication and IFN-beta induction was also determined. It was found that the severity of the diabetes and the amount of IFN-beta produced was dependent on the cell line used for virus propagation. Virus synthesis was augmented and IFN-beta production was altered in insulin-treated cell cultures. It is concluded that D virus either consists of more than one virus or that its diabetes and IFN-beta inducing characteristics are unstable.

Adult male ICR Swiss mice develop diabetes mellitus when infected with the D variant of encephalomyocarditis virus. It was determined that the disease syndrome caused by the virus in this mouse strain is dependent upon the age of the animals. Mice younger than 7 weeks developed lethal encephalitis, whereas those past this age developed diabetes. The susceptibility of young mice to the diabetogenic effects of encephalomyocarditis virus was enhanced by testosterone.