Anita Kondrashova1, Noora Nurminen1, Maarit Patrikainen1, Heini Huhtala2, Jussi Lehtonen1, Jorma Toppari3,4, Jorma Ilonen5,6, Olli G Simell4, Riitta Veijola7, Mikael Knip8,9,10,11, Heikki Hyöty12,13. 1. School of Medicine, University of Tampere, Biokatu 10, FIN-33520, Tampere, Finland. 2. School of Health Sciences, University of Tampere, Tampere, Finland. 3. Department of Physiology, University of Turku, Turku, Finland. 4. Department of Pediatrics, Turku University Hospital, Turku, Finland. 5. Department of Clinical Microbiology, University of Eastern Finland, Kuopio, Finland. 6. Immunogenetics Laboratory, University of Turku, Turku, Finland. 7. Department of Pediatrics, University of Oulu, Oulu, Finland. 8. Children's Hospital, University of Helsinki and Helsinki University Hospital, Helsinki, Finland. 9. Research Programs Unit, Diabetes and Obesity, University of Helsinki, Helsinki, Finland. 10. Folkhälsan Research Center, Helsinki, Finland. 11. Tampere Center for Child Health Research, Tampere University Hospital, Tampere, Finland. 12. School of Medicine, University of Tampere, Biokatu 10, FIN-33520, Tampere, Finland. Heikki.Hyoty@uta.fi. 13. Fimlab Laboratories, Pirkanmaa Hospital District, Tampere, Finland. Heikki.Hyoty@uta.fi.
Abstract
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.
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.
Entities:
Keywords:
Influenza A virus; Type 1 diabetes; Virus antibodies
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