Relationship of interferon-inducing particle phenotype to encephalomyocarditis virus-induced diabetes mellitus

Abstract

The B (nondiabetogenic) and D (diabetogenic) variants of encephalomyocarditis (EMC) virus were studied to further define the role of the interferon (IFN) system in murine virus-induced diabetes mellitus. The relationship between the initial multiplicity of infection with EMC-B and the IFN yield showed that cells infected with one IFN-inducing particle produce a maximum amount of IFN, whereas IFN production is suppressed in cells infected with two or more particles. The IFN yield induced by EMC-D was less than 5% of that induced by EMC-B, allowing the designation of the B and D variants as Ifp+ and Ifp-, respectively. The Ifp+ property of the virion was shown to be responsible for the greater sensitivity of EMC-B to exogenous IFN as a result of primed local IFN induction. The data indicate that different Ifp phenotypes occur in nature and are associated with the development of diabetes in mice.