| 1. |
- Lindehammer, Sabina Resic, et al.
(författare)
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Viruses, diabetes, and autoimmunity : Studies of subjects at genetic risk for type 1 diabetes
- 2013
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Ingår i: Diabetes and Viruses. - New York, NY : Springer New York. - 9781461440505 - 9781461440512 ; 9781461440512, s. 187-194
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Bokkapitel (refereegranskat)abstract
- The possible importance of virus infections before the development of islet autoimmunity and then for the appearance of clinical type 1 diabetes is reviewed. There is a lack of specific data on the role of virus to induce islet autoimmunity. There is also a paucity of data to demonstrate that virus infections may contribute to an accelerated disease process resulting in clinical onset of type 1 diabetes. In contrast, there is a plethora of studies on virus infections at the time of clinical onset. However, these studies have made the understanding of virus in type 1 diabetes less easy. Future studies need to address further gestational infections and the risk of the offspring for islet autoimmunity. Such studies should also investigate the mechanisms by which gestational infections may alter the ability of the offspring to respond to future virus infections related to the development of islet autoimmunity or accelerator of the clinical onset of diabetes.
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| 2. |
- Rešić Lindehammer, Sabina, et al.
(författare)
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Seroconversion to Islet Autoantibodies After Enterovirus Infection in Early Pregnancy.
- 2012
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Ingår i: Viral Immunology. - : Mary Ann Liebert Inc. - 0882-8245 .- 1557-8976. ; 25:4, s. 254-261
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Tidskriftsartikel (refereegranskat)abstract
- Gestational enterovirus (EV) infections have been associated with an increased risk for type 1 diabetes in the offspring. We therefore analyzed non-diabetic mothers for EV exposure in early pregnancy in relation to type 1 diabetes HLA-DQ risk genotypes and seroconversion to islet autoantibodies during pregnancy. Non-diabetic mothers who had islet autoantibodies (n=365) against glutamic acid decarboxylase (GADA), islet antigen-2 autoantibodies (IA-2A), or insulin autoantibodies (IAA), in early pregnancy and at delivery were compared to islet autoantibody-negative mothers (n=1457) matched for age and sampling date. Mothers were genotyped for HLA-DQ and analyzed for both EV-RNA and EV-IgM. EV-IgM, but not EV-RNA, was detected during early pregnancy in 12% of islet autoantibody-positive mothers compared to 11% of the controls. In early pregnancy, mothers with HLA-DQ 2/2 or 2/X genotypes showed an increased risk for islet autoantibodies at delivery (OR 1.85; p=0.001). After adjusting for parity, maternal age, year of birth, and season of early pregnancy, early pregnancy EV-IgM combined with DQ2/2 or 2/X increased the risk for islet autoantibodies (OR 3.10; 95% CI 1; p=0.008). EV-IgM in early pregnancy increased the risk for islet autoantibodies at delivery in non-diabetic mothers with HLA-DQ 2/2 or 2/X type 1 diabetes risk genotypes.
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