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Diabetes mellitus due to viruses--some recent developments
T M Szopa1, P A Titchener, N D Portwood
1Medical Unit, Royal London Hospital, UK.
Abstract:
Many different viruses belonging to several genera have the potential to damage beta cells. The mechanisms they employ are varied, and infection may result in either a direct destruction of islets and rapid insulin deficiency, or in a more gradual loss of functioning islets with the onset of diabetes many years later. Several case histories involving extensive cytolysis of beta cells can be directly linked to viral infection, whilst an example of diabetes occurring many years after viral infection is found in individuals who had a congenital infection with rubella virus. Here, the virus induces an autoimmune reaction against beta cells. Autoimmune phenomena have also been observed in islets following infections with viruses other than rubella, and thus activation of autoimmune mechanisms leading to beta-cell destruction may be a relatively frequent occurrence. Recent evidence shows that picornaviruses are not exclusively lytic, and can induce more subtle, long-term changes in beta cells, which may be important in the aetiology of diabetes. The exact mechanisms involved are not known, but it is clear that several viruses can directly inhibit insulin synthesis and induce the expression of other proteins such as interferons, and the HLA antigens. Strain differences in viruses are important since not all variants are tropic for the beta cells. Several laboratories are in the process of identifying the genetic determinants of tropism and diabetogenicity, especially amongst the Coxsackie B (CB) virus group. The sequence of one such diabetogenic CB4 strain virus has been determined.(ABSTRACT TRUNCATED AT 250 WORDS)
Insights
Viral infections can lead to diabetes by directly destroying beta cells or triggering autoimmune responses. Research is ongoing to understand the specific viral mechanisms and genetic factors involved in beta cell damage and diabetes development.
Area of Science:
- Virology
- Immunology
- Endocrinology
Background:
- Viruses can damage pancreatic beta cells, leading to insulin deficiency and diabetes.
- Viral infections can cause direct beta cell destruction or trigger autoimmune reactions.
- Long-term effects of viral infections, like congenital rubella, can manifest as diabetes years later.
Purpose of the Study:
- To explore the diverse mechanisms by which viruses damage beta cells.
- To investigate the role of viral infections in the etiology of diabetes.
- To identify genetic factors in viruses that determine tropism and diabetogenicity.
Main Methods:
- Review of case histories linking viral infections to beta cell cytolysis.
- Analysis of autoimmune phenomena in islets following viral infections.
- Investigation of picornaviruses' non-lytic effects on beta cells.
- Genetic sequencing of diabetogenic Coxsackie B virus strains.
Main Results:
- Viral infections can cause rapid or gradual beta cell loss, resulting in diabetes.
- Autoimmune responses against beta cells are frequently triggered by viral infections.
- Some viruses inhibit insulin synthesis and alter protein expression (e.g., interferons, HLA antigens).
Conclusions:
- Multiple viruses can induce diabetes through direct damage or autoimmune mechanisms.
- Understanding viral tropism and diabetogenicity is crucial for diabetes research.
- Further research into viral genetic determinants will elucidate diabetes pathogenesis.