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Effect of interferon on encephalomyocarditis virus infection of cultured mouse pancreatic B cells
Abstract:
The M variant of encephalomyocarditis virus (EMC) produces a disease similar to human insulin-dependent diabetes mellitus in some but not all strains of mice. This diabetogenic M variant was found to induce fivefold more interferon than non-diabetogenic strains of EMC in cultures of mouse L 929 fibroblasts. When interferon induced by the M variant was added to monolayers of B cells from both diabetes-'susceptible' CD-1 mice and 'resistant' C57 bl/6 mice before EMC infection, B cell damage and virus replication were delayed. In addition, viral production in B cell cultures from C57 bl/6 mice was reduced five- to tenfold. A similar effect was not found when cultures from CD-1 mice were treated with interferon. Thus, interferon might play an important role in modulating the severity of the initial infection of B cells.
Insights
Encephalomyocarditis virus (EMC) M variant induces more interferon, which delays B cell damage and viral replication in some mice. This suggests interferon modulates initial EMC infection severity.
Area of Science:
- Virology
- Immunology
- Endocrinology
Background:
- Encephalomyocarditis virus (EMC) M variant causes diabetes-like disease in susceptible mice.
- The diabetogenic M variant induces significantly more interferon than non-diabetogenic strains.
- Interferon's role in EMC-induced diabetes pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the role of interferon in modulating B cell response to EMC infection.
- To compare the effects of EMC-induced interferon on B cells from diabetes-susceptible and resistant mouse strains.
Main Methods:
- Culturing mouse L 929 fibroblasts to assess interferon induction by EMC variants.
- Treating B cell cultures from CD-1 (susceptible) and C57 bl/6 (resistant) mice with EMC-induced interferon prior to infection.
- Measuring B cell damage and viral replication in treated and untreated B cell cultures.
Main Results:
- Interferon induced by the EMC M variant was fivefold higher than non-diabetogenic strains.
- Pre-treatment with EMC-induced interferon delayed B cell damage and viral replication in both susceptible and resistant mouse strains.
- Viral production was reduced five- to tenfold in resistant C57 bl/6 mouse B cells, but not in susceptible CD-1 mouse B cells.
- Interferon treatment did not show a similar protective effect in CD-1 mouse B cells.
Conclusions:
- Interferon plays a significant role in modulating the initial B cell response to encephalomyocarditis virus infection.
- Mouse strain differences in interferon response may contribute to varying susceptibility to EMC-induced diabetes.
- Further research is warranted to elucidate the precise mechanisms of interferon's protective effects in resistant mouse strains.