A mild diabetes was induced in mice following the inoculation of a myocardial variant of encephalomyocarditis virus. The majority of infected mice developed a transient hyperglycaemia and only a few mice exhibited a chronic elevation of blood glucose. Infected mice were selected for study if their non-fasting blood glucose levels were above two standard deviations of values in control mice for at least 5 consecutive days. The pancreas from selected inoculated mice and control mice was removed 60 days after infection; random blood glucose levels at this time had returned to normal. Isolated islets of Langerhans from such previously ‘diabetic’ mice were used to determine the rate of insulin secretion, insulin biosynthesis and cyclic AMP accumulation in response to various glucose concentrations. At glucose (16 mmol/l), both insulin release and biosynthesis were depressed in previously infected animals. At glucose (2 and 10 mmol/l), while insulin biosynthesis was unchanged in infected animals, insulin release was increased. Cyclic AMP accumulation in response to glucose (20 mmol/l) was found to be significantly elevated in islets from infected animals and especially in response to glucose (20 mmol/l) in the presence of isobutyl methyl xanthine (1 mmol/l). Infected mice exhibited a reduction of total pancreatic insulin content in comparison with control mice. The insulin content of isolated islets of Langerhans from infected and control mice was found to be the same. Serum insulin levels, however, from infected mice were higher than in control sera. The results suggest that the myocardial variant of encephalomyocarditis virus in certain inbred strains of mice causes alteration in some of the biochemical functions of the B cells, 60 days after infection. It is not known, however, how permanent these alterations are.