Viruses, diabetes, and autoimmunity : Studies of subjects at genetic risk for type 1 diabetes

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

Temporal trends of HLA genotype frequencies of type 1 diabetes patients in Sweden from 1986 to 2005 suggest altered risk.

The aim of this study was to compare the frequency of human leukocyte antigen (HLA) genotypes in 1-18-year-old patients with type 1 diabetes newly diagnosed in 1986-1987 (n = 430), 1996-2000 (n = 342) and in 2003-2005 (n = 171). We tested the hypothesis that the HLA DQ genotype distribution changes over time. Swedish type 1 diabetes patients and controls were typed for HLA using polymerase chain reaction amplification and allele specific probes for DQ A1* and B1* alleles. The most common type 1 diabetes HLA DQA1*-B1*genotype 0501-0201/0301-0302 was 36% (153/430) in 1986-1987 and 37% (127/342) in 1996-2000, but decreased to 19% (33/171) in 2003-2005 (P 0.05). This study in 1-18-year-old Swedish type 1 diabetes patients supports the notion that there is a temporal change in HLA risk