Relationship of interferon-inducing particle phenotype to encephalomyocarditis virus-induced diabetes mellitus.
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.
D000818:Animals; D002478:Cells, Cultured; D003921:Diabetes Mellitus, Experimental / Q000276:immunology / Q000382:microbiology*; D004622:Embryo, Mammalian; D004686:Encephalomyocarditis virus / Q000472:pathogenicity*; D014644:Genetic Variation; D007370:Interferon Type I / Q000235:genetics*; D007700:Kinetics; D007739:L Cells / Q000187:drug effects / Q000276:immunology; D051379:Mice; D011070:Poly I-C / Q000494:pharmacology; D010948:Viral Plaque Assay
D007370:Interferon Type I; D011070:Poly I-C