Coxsackie virus B4 produces transient diabetes in nonhuman primates.
Cynomolgus, rhesus, and Cebus monkeys failed to show glucose tolerance or insulin secretion abnormalities after infection with encephalomyocarditis virus or Coxsackie virus B4. Patas monkeys also showed no abnormalities after infection with encephalomyocarditis virus. However, patas monkeys infected with Coxsackie virus B4 or treated first with a subdiabetogenic dose of streptozocin and then infected sequentially with Coxsackie viruses B4 and B3 showed transient elevation of glucose tolerance tests, depressed insulin secretion, and glucose in the urine. Our experiments in nonhuman primates support earlier studies in mice and humans that under certain circumstances, Coxsackie viruses can cause abnormalities in glucose homeostasis.
D000818:Animals; D003384:Coxsackievirus Infections / Q000150:complications* / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000209:etiology*; D003922:Diabetes Mellitus, Type 1 / Q000209:etiology*; D029822:Enterovirus B, Human; D005947:Glucose / Q000378:metabolism; D000882:Haplorhini; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D013045:Species Specificity
D007328:Insulin; D005947:Glucose