Abstract
INFECTION of certain inbred strains of mice with the M variant of encephalomyocarditis (EMC) virus produces β-cell damage and a diabetes-like syndrome1–4. The development of this syndrome is genetically determined and susceptibility is inherited as an autosomal recessive trait5,6. The genetic factors involved seem to act at the level of the β cells, and in vitro studies have shown that β cells from susceptible strains of mice are more permissive to EMC infection than β cells from resistant strains of mice7. We have investigated first, the capacity of EMC virus to replicate in β cells from F1 and F2 offspring of susceptible and resistant strains of mice, and second, the effect of the viral infection on the level of insulin and glucose in the blood.
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