Coxsackie B4 virus induces short‐term changes in the metabolic functions of mouse pancreatic islets in vitro

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Abstract
Mouse pancreatic islets cultured in vitro were infected with a tissue culture-adapted or a mouse pancreas-adapted strain of Coxsackie B4 (CB4) virus. The effects of the viruses on the islets were assessed by examination of their biochemical functions. It was found that the mouse pancreas-adapted strain of CB4 induced a ‘leakage’ of insulin from islets incubated at a basal (2 mmol l−1) glucose concentration, both at two and four days following infection. However, at a stimulatory concentration of glucose (20 mmol l−1) the rate of insulin secretion appeared to be normal in these islets. At two days the rate of total protein synthesis in islets infected with mouse pancreas-adapted CB4, incubated at high glucose concentration, was reduced; at four days the degree of inhibition was more severe, the rate at basal glucose concentration falling to half that of the control islets and at the stimulatory glucose concentration to a quarter of the control islets. (Pro)insulin biosynthesis was also inhibited, the rate being reduced to less than half the mean control value in islets infected with mouse pancreas-adapted CB4 virus at 20 mmol l−1 glucose at two days; at four days the rate was greatly reduced at both 2 and 20 mmol l−1 glucose. It is concluded from this study that (1) only certain strains of CB4 virus can infect mouse pancreatic islets in vitro and (2) that infection with strains of virus tropic for the islets leads to an impairment of metabolic functions of the B-cells, and is not necessarily lytic.