期刊
DIABETOLOGIA
卷 58, 期 11, 页码 2592-2595出版社
SPRINGER
DOI: 10.1007/s00125-015-3723-4
关键词
Influenza A virus; Type 1 diabetes; Virus antibodies
资金
- Diabetes Research Foundation in Finland
- Sigrid Juselius Foundation
- Competitive Research Funding of the Tampere University Hospital
- Juvenile Diabetes Research Foundation (JDRF)
- Academy of Finland
- Paivikki and Sakari Sohlberg's Foundation
Aims/hypothesis Viral infections have long been considered potential triggers of beta cell autoimmunity and type 1 diabetes. Recent studies have suggested that influenza A virus might increase the risk of type 1 diabetes. The present study evaluates this risk association in prospectively observed children at the time when islet autoimmunity starts and autoantibodies are first detected. Methods IgG class antibodies to influenza A virus were analysed in 95 case children whose antibody screening test turned permanently positive for two or more islet autoantibodies and from 186 autoantibody-negative and non-diabetic control children who were matched for time of birth, sex, date of sampling and HLA-conferred risk of diabetes in the Finnish Type 1 Diabetes Prediction and Prevention (DIPP) study. Virus antibodies were measured from the first autoantibody-positive sample using an enzyme immunoassay. None of the children had been vaccinated against influenza A. Results The prevalence of influenza A virus antibodies did not differ between the case and control children (42% vs 38%; p = 0.392) and the median antibody levels were also comparable in the two groups (3.0 vs 3.8 enzyme immunoassay units). A similar result was obtained when case and control children were compared separately in subgroups according to different sex, age and HLA-DQ genotype. However, girls had higher antibody levels than boys among both case and control children (median antibody levels 9.0 vs 2.3 enzyme immunoassay units; p = 0.01). Conclusions/interpretation Our results suggest that influenza A infections are not associated with the development of islet autoimmunity in young children with increased genetic susceptibility to type 1 diabetes.
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