Abstract
Encephalomyocarditis (EMC) virus, Mengovirus 2T and Coxsackie virus B4 can induce diabetes in mice by infecting and destroying pancreatic beta cells. The destruction of beta cells in EMC virus-infected mice is not dependent on the immune responses but the genetic background of the host and genetic makeup of the virus. In addition to the acute metabolic alterations, mice with diabetes for six months show some long-term complications, including glomerulosclerosis, ocular changes and decreased bone formation and mineralization. EMC virus-induced diabetes in mice can be prevented by interferon and/or a live attenuated vaccine. In contrast to EMC induced diabetes, reovirus type I may cause a polyendocrine disease characterized by a mild and transient type of diabetes that can be prevented by immunosuppression. It is concluded that there are at least two different pathogenic mechanisms for virus-induced diabetes in mice: the one is direct cytolytic infection of beta cells and the other is the autoimmune mediated destruction of beta cells.
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© 1987 Martinus Nijhoff Publishing, Boston
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Yoon, JW. (1987). Virus-Induced Diabetes in Mice. In: Becker, Y. (eds) Virus Infections and Diabetes Mellitus. Developments in Medical Virology, vol 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2085-2_13
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DOI: https://doi.org/10.1007/978-1-4613-2085-2_13
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