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Possible mechanisms in the pathogenesis of virus-induced diabetes mellitus
1Department of Microbiology and Infectious Diseases, Julia McFarlane Diabetes Research Unit, University of Calgary, Alberta, Canada.
Abstract:
Insulin-dependent diabetes mellitus results from destruction of pancreatic beta cells. Viruses and autoimmunity have been implicated as possible causes of beta cell destruction in genetically predisposed individuals. The evidence for viruses comes largely from experiments in animals, but several studies in humans point to viruses as triggers in the pathogenesis of diabetes in some cases. In animal models, at least 4 different possible mechanisms for virus-induced diabetes have been proposed. The first mechanism is direct cytolytic infection of pancreatic beta cells. One group of viruses, including encephalomyocarditis virus, Mengovirus 2T, and Coxsackie B viruses, can directly infect and destroy pancreatic beta cells independent of autoimmune processes. The second mechanism is triggering of autoimmune responses. In contrast to the encephalomyocarditis virus-induced diabetes, reovirus type 1 and rubella virus seem to be somehow associated with autoimmunity in the genesis of a diabetes-like syndrome in a certain strain of suckling mice and hamsters, respectively. The third mechanism is cumulative environmental insults. The cumulative environmental insults with viruses and beta cell toxic chemicals can result in diabetes in genetically predisposed non-human primates and certain inbred strains of mice. The fourth mechanism is persistent infection. A certain virus, such as lymphocytic choriomeningitis virus, persistently infects murine pancreatic beta cells and produces hyperglycemia. The evidence that viruses cause diabetes in humans is more circumstantial.(ABSTRACT TRUNCATED AT 250 WORDS)
Insights
Viruses may trigger insulin-dependent diabetes by directly destroying pancreatic beta cells or by initiating autoimmune responses in genetically susceptible individuals. Animal studies reveal multiple viral mechanisms contributing to diabetes pathogenesis.
Area of Science:
- Virology
- Immunology
- Endocrinology
Background:
- Insulin-dependent diabetes mellitus (IDDM) arises from pancreatic beta cell destruction.
- Both viral infections and autoimmunity are implicated in IDDM pathogenesis, particularly in genetically predisposed individuals.
Purpose of the Study:
- To review proposed mechanisms by which viruses may induce diabetes.
- To explore the role of viruses in beta cell destruction and diabetes development.
Main Methods:
- Review of existing animal model studies and human epidemiological data.
- Analysis of proposed viral mechanisms including direct cytolysis, autoimmunity induction, cumulative insults, and persistent infection.
Main Results:
- Animal models demonstrate viruses can directly infect and destroy beta cells (e.g., encephalomyocarditis virus).
- Viruses can trigger autoimmune responses leading to diabetes-like syndromes (e.g., reovirus type 1, rubella virus).
- Cumulative environmental factors and persistent viral infections also contribute to diabetes in animal models.
Conclusions:
- Viruses represent a potential etiological factor in human diabetes, though evidence is largely circumstantial.
- Multiple mechanisms illustrate the complex interplay between viruses, host genetics, and immune responses in diabetes development.