Transient diabetes following chicken pox.
ABSTRACT The paper describes two individuals presenting with acute insulin dependent diabetes mellitus for a brief and transient period. Both had had chicken pox infection in the immediate past. After establishing good diabetic control, insulin was withdrawn over a few weeks. Follow-up for the next two years did not reveal recurrence of diabetes. A causal relation between varicella zoster virus and the onset of diabetes is suggested.
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ABSTRACT: There is a consensus among epidemiologists that the worldwide incidence rate of type 1 diabetes has been rising in recent decades. The cause of this rise is unknown, but epidemiological studies suggest the involvement of environmental factors, and viral infections in particular. Data demonstrating a cause-and-effect relationship between microbial infections and type 1 diabetes and how viruses may cause disease in humans are currently lacking. However, new evidence from animal models supports the hypothesis that viruses induce disease via mechanisms linked with innate immune upregulation. In the BioBreeding Diabetes Resistant rat, infection with a parvovirus induces islet destruction via upregulation of the toll-like receptor 9 (TLR9) signaling pathway. Data from mouse models of diabetes implicate TLR2, TLR3, and TLR7 in the disease process. Understanding the link between environmental agents and innate immune pathways involved in early stages of diabetes may advance the design of immune interventions to prevent disease in genetically susceptible individuals.Clinical Immunology 04/2009; DOI:10.1016/j.clim.2008.12.011 · 3.99 Impact Factor
- Diabetes / Metabolism Reviews 07/1995; 11(2):83-107. DOI:10.1002/dmr.5610110202
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ABSTRACT: Type 1 diabetes (T1D) results from the destruction of pancreatic beta cells. Genetic factors are believed to be a major component for the development of T1D, but the concordance rate for the development of diabetes in identical twins is only about 40%, suggesting that nongenetic factors play an important role in the expression of the disease. Viruses are one environmental factor that is implicated in the pathogenesis of T1D. To date, 14 different viruses have been reported to be associated with the development of T1D in humans and animal models. Viruses may be involved in the pathogenesis of T1D in at least two distinct ways: by inducing beta cell-specific autoimmunity, with or without infection of the beta cells, [e.g. Kilham rat virus (KRV)] and by cytolytic infection and destruction of the beta cells (e.g. encephalomyocarditis virus in mice). With respect to virus-mediated autoimmunity, retrovirus, reovirus, KRV, bovine viral diarrhoea-mucosal disease virus, mumps virus, rubella virus, cytomegalovirus and Epstein-Barr virus (EBV) are discussed. With respect to the destruction of beta cells by cytolytic infection, encephalomyocarditis virus, mengovirus and Coxsackie B viruses are discussed. In addition, a review of transgenic animal models for virus-induced autoimmune diabetes is included, particularly with regard to lymphocytic choriomeningitis virus, influenza viral proteins and the Epstein-Barr viral receptor. Finally, the prevention of autoimmune diabetes by infection of viruses such as lymphocytic choriomeningitis virus is discussed.Diabetes/Metabolism Research and Reviews 01/2003; 19(1):8-31. DOI:10.1002/dmrr.337 · 2.97 Impact Factor