The D variant of encephalomyocarditis (EMC-D) virus does not induce the production of interferon (IFN) and produces an insulin-dependent diabetes mellitus (IDDM)-like syndrome in certain mouse strains. In contrast, the B variant (EMC-B) virus, which is serologically identical to EMC-D virus, is a good inducer of IFN and is nondiabetogenic. It has been postulated that IFN may play a major role in determining the ability of these two viruses to infect pancreatic β-cells. However, recent studies have shown that ICR Swiss and BALB/cByJ male mice are not protected by IFN against EMC-D virus-induced IDDM. Furthermore, treatment of these two strains of mice with anti-IFN γ-globulin before infection with EMC-B virus does not result in diabetes. These observations suggest that mechanisms other than the IFN system are involved in determining the ability of the viruses to infect and destroy β-cells. Studies were initiated to identify other mechanisms of action. In this communication, we show that up to six times more EMC-D than EMC-B virus attaches to primary β-cells extracted from male ICR Swiss mice. This difference in ability to attach to β-cells may account for the difference in the diabetic potential of this mouse strain.

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