Levels of insulin mRNA in pancreata from SJL/J male mice susceptible to encephalomyocarditis (EMC)-D virus-induced diabetes started to decrease rapidly 24 h after injection with EMC-D virus and only a trace remained 72 h after injection. In contrast, insulin mRNA in pancreata from C57BL/6J male mice resistant to EMC-D virus-induced diabetes did not show any significant changes 0 to 96 h after injection. EMC-D viral RNA in pancreata from SJL/J mice started to increase rapidly 24 h after injection, reached its peak at 48 h and then decreased gradually. In contrast, EMC-D viral RNA in pancreata from C57BL/6J mice was undetectable except for the 24 and 48 h points after injection. EMC-D virus could bind readily to freshly isolated beta cells from SJL/J mice but scarcely bound to beta cells from C57BL/6J mice. In contrast, there was no significant difference between SJL/J and C57BL/6J mice in binding of EMC-D virus to their cultured beta cells. The rate of EMC-D viral attachment to beta cells from C57BL/6J mice increased significantly during the first 24 h culture period and reached the same rate of attachment as that seen for beta cells from SJL/J mice. This suggests that viral receptors on the beta cells derived from strains of mice resistant to EMC virus-induced diabetes are not expressed , but are expressed during cell culture, rendering the beta cells susceptible to EMC viral infection. On the basis of our previous and present observations, we conclude that a genetic factor controlling susceptibility to EMC-D virus-induced diabetes may operate by modulating the expression of viral receptors on the beta cells.


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