The importance of immunologic factors in the pathogenesis of encephalomyocarditis virus induced diabetes in mice.

The pathogenesis of EMC virus induced diabetes has generally been thought to be caused by direct cytopathic effect of the virus on beta cells with susceptibility or resistance dictated primarily by the density of viral receptors on the beta cells of different individuals. The histological finding of insulitis, our demonstration of a protective effect of immunosuppression with ALS or anti-theta antibody and silica supports host immune factors as important determinants of susceptibility. A critical role of the immune system might be mediated by autoimmune destruction of EMC-virus infected beta cells. In susceptible strain mice treated with low dose cyclophosphamide to deplete suppressor cells, which may halt the autoimmune process and allow recovery, a prolonged period of hyperglycemia was demonstrated as compared to controls. Bone marrow exchanged between susceptible and resistant strains was also found to alter susceptibility. "B mice", deficient in T lymphocytes, when infected with EMC virus had a decreased incidence of diabetes. Susceptibility to EMC diabetes may be dictated by the autoaggressive response of host immune system to beta cells altered by EMC virus infection.