The D variant of encephalomyocarditis virus (EMC-D) infects pancreatic beta cells in susceptible mouse strains producing a disease syndrome similar to insulin-dependent diabetes in humans (5,11). We have recently reported that EMC-D replicates primarily in the pancreas and spleen of ICR Swiss male mice, and to a lesser extent in the heart and lung tissues (8). Interferon (IFN) or IFN-inducers have been shown to protect some, but not all, susceptible mouse strains against the diabetogenic effects of EMC-D (2,3,11). For example, SWR/J mice respond well to the protective effects of IFN, while ICR Swiss animals are not protected (3). We have been studying the role of IFN on the development of virus-induced murine diabetes. Since IFNs have been shown to be powerful immune modulators (9,10) it was the purpose of the present study to determine if IFN given after infection by EMC-D had any effect on the frequency or severity of diabetes in susceptible ICR Swiss and resistant C57B1/6 mice. Virus replication in selected tissues was also determined. The data presented show that IFN exacerbates the severity of diabetes caused by the virus in ICR Swiss mice and induces the diabetic state in the otherwise resistant C57B1/6 animals.
- Standard Deviation
- Post Infection
- Diabetic State
- Pancreatic Beta Cell
- Plaque Form Unit
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Gould, C.L., McMannama, K.G., Bigley, N.J., Giron, D.J. (1986). Exacerbation of the Pathogenesis of the Diabetogenic Variant of Encephalomyocarditis Virus in Mice by Interferon. In: Szentivanyi, A., Friedman, H. (eds) Viruses, Immunity, and Immunodeficiency. University of South Florida International Biomedical Symposia Series. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2185-9_29
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