Exacerbation of the pathogenesis of the diabetogenic variant of encephalomyocarditis virus in mice by interferon.
Adult male ICR Swiss mice develop insulin-dependent diabetes when infected with the D variant of encephalomyocarditis virus (EMC-D). In contrast, adult C57Bl/6 males are relatively resistant to the diabetogenic effects of this virus. We have been studying the role of interferon (IFN) in the pathogenesis of infection by EMC-D and development of virus-induced murine diabetes mellitus. The data show that when IFN beta or IFN gamma were administered four days after virus infection, the frequency and severity of diabetes were exacerbated in ICR Swiss mice, and the diabetic state was induced in the resistant C57Bl/6 strain. In addition, animals treated with either of the IFNs or the IFN-inducer poly I:C, developed symptoms of severe encephalomyocarditis. Analysis of ICR Swiss mouse tissues revealed that IFN-treatment resulted in virus replication in the heart and brain and the reappearance of the virus in the pancreas. It is concluded that under certain conditions, the diabetic state is exacerbated and the normal course of (EMC-D)-infection in mice is altered by IFN.
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000209:etiology / Q000382:microbiology*; D004769:Enterovirus Infections / Q000150:complications* / Q000628:therapy; D006321:Heart / Q000382:microbiology; D007370:Interferon Type I / Q000494:pharmacology*; D007515:Islets of Langerhans / Q000382:microbiology; D004680:Maus Elberfeld virus; D051379:Mice; D008815:Mice, Inbred Strains; D011070:Poly I-C / Q000494:pharmacology; D014779:Virus Replication / Q000187:drug effects
D007370:Interferon Type I; D011070:Poly I-C