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Genetic influences on the immunologic pathogenesis of encephalomyocarditis (EMC) virus-induced diabetes mellitus
Abstract:
DBA/2 and Balb/cBY mice were infected with approximately 30 plaque-forming units of the M-variant of encephalomyocarditis (EMC-M) virus. Seven days after inoculation the majority of the animals of both strains were hyperglycemic. A significant correlation between increased concentrations of virus in the pancreas and hyperglycemia was found among individual DBA/2 animals, but not among Balb/cBY mice. T-lymphocyte depletion of DBA/2 mice before infection failed to alter the incidence or severity of hyperglycemia in comparison to intact animals. Conversely, hyperglycemia in T-lymphocyte-depleted Balb/cBY mice was reduced substantially in comparison to infected immunocompetent animals. There appears to be at least two genetically influenced pathogenic mechanisms of diabetes in EMC-M virus-infected mice. In some strains of animals, hyperglycemia results exclusively from viral infection and the consequent injury to the beta cells, whereas in other animals, viral damage to the islets is compounded by immunologic events.
Insights
Encephalomyocarditis virus (EMC-M) infection causes hyperglycemia in mice through distinct mechanisms. Some strains develop diabetes solely from viral beta-cell injury, while others involve immune responses.
Area of Science:
- Virology
- Immunology
- Endocrinology
Background:
- Encephalomyocarditis virus (EMC-M) can induce hyperglycemia in susceptible animal models.
- The pathogenesis of virus-induced diabetes mellitus is complex and may involve genetic factors.
- Understanding the interplay between viral infection and host immune responses is crucial for elucidating diabetes mechanisms.
Purpose of the Study:
- To investigate the mechanisms underlying hyperglycemia in DBA/2 and Balb/cBY mice infected with EMC-M virus.
- To determine the role of T-lymphocytes in the development of virus-induced hyperglycemia in different mouse strains.
Main Methods:
- DBA/2 and Balb/cBY mice were infected with EMC-M virus.
- Hyperglycemia was assessed seven days post-inoculation.
- T-lymphocyte depletion was performed in a subset of mice prior to infection.
- Viral load in the pancreas and its correlation with hyperglycemia were analyzed.
Main Results:
- Both mouse strains exhibited hyperglycemia post-infection.
- A correlation between pancreatic viral load and hyperglycemia was observed in DBA/2 mice but not Balb/cBY mice.
- T-lymphocyte depletion did not affect hyperglycemia in DBA/2 mice.
- Hyperglycemia was significantly reduced in T-lymphocyte-depleted Balb/cBY mice compared to immunocompetent controls.
Conclusions:
- Two distinct pathogenic mechanisms for EMC-M virus-induced diabetes exist in mice, influenced by genetic background.
- In DBA/2 mice, hyperglycemia appears to result directly from viral beta-cell injury.
- In Balb/cBY mice, hyperglycemia involves both viral damage and a compounded immunologic response, modulated by T-lymphocytes.