Influenza A virus antibodies show no association with pancreatic islet autoantibodies in children genetically predisposed to type 1 diabetes

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.

Pandemic influenza and subsequent risk of type 1 diabetes: a nationwide cohort study

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Nonobese Diabetic (NOD) Mice Lack a Protective B-Cell Response against the “Nonlethal”Plasmodium yoelii17XNL Malaria Protozoan

“…Recently, it has been shown that the influenza virus infection does not impair the antiviral immune response in NOD mice [36]. Also, human studies showed no significant difference in the titers of anti-influenza viral antibodies between nonvaccinated, genetically predisposed children to T1D and control children [37]. Our study showed that in the case of P. yoelii 17XNL infection, the NOD mice are unable to mount an anti-parasite antibody response, which infers our previous hypothesis that a major mechanism of immune evasion by malaria parasites relies on suppression of B-cell function throughout induction of parasite-specific Foxp3 + Treg cells [38].…”