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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.
Insights
Encephalomyocarditis virus variants impact interferon production. The non-diabetogenic EMC-B virus induces more interferon than the diabetogenic EMC-D, influencing diabetes development in mice.
Area of Science:
- Virology
- Immunology
- Endocrinology
Background:
- The interferon (IFN) system plays a crucial role in antiviral defense.
- Encephalomyocarditis virus (EMC) can induce diabetes mellitus in mice.
- Understanding the interplay between EMC virus variants and the IFN system is key to understanding virus-induced diabetes.
Purpose of the Study:
- To investigate the role of the interferon (IFN) system in murine virus-induced diabetes mellitus.
- To characterize the differences in IFN induction between the nondiabetogenic EMC-B and diabetogenic EMC-D virus variants.
- To determine the significance of the IFN-inducing property (Ifp) of EMC virus in disease pathogenesis.
Main Methods:
- Comparative analysis of IFN production following infection with EMC-B and EMC-D variants.
- Assessment of the relationship between initial viral multiplicity of infection and IFN yield.
- Evaluation of the sensitivity of EMC-B and EMC-D to exogenous IFN.
- Determination of the Ifp phenotype of EMC variants.
Main Results:
- EMC-B, the nondiabetogenic variant, induced significantly higher IFN yields compared to EMC-D, the diabetogenic variant (EMC-D induced <5% of EMC-B's IFN yield).
- A single IFN-inducing particle maximized IFN production; higher multiplicities suppressed IFN yield.
- EMC-B was designated Ifp+ and EMC-D as Ifp- based on IFN induction levels.
- The Ifp+ property of EMC-B correlated with increased sensitivity to exogenous IFN due to primed local IFN induction.
Conclusions:
- Different Ifp phenotypes of EMC virus exist naturally.
- The Ifp phenotype of EMC virus is directly associated with its diabetogenic potential in mice.
- The IFN system's modulation by EMC virus variants is a critical factor in the development of virus-induced diabetes mellitus.