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Pediatr Infect Dis J. 2018 Oct 19. doi: 10.1097/INF.0000000000002201. [Epub ahead of print]

No Association Between Ljungan Virus Seropositivity and the Beta-Cell Damaging Process in the Finnish Type 1 Diabetes Prediction and Prevention Study Cohort.

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Helsinki University and Helsinki University Hospital (HUSLAB), Department of Virology, Finland.
Department of Virology, School of Medicine, University of Tampere, Tampere, Finland.
Department of Virology, University of Turku, Turku, Finland.
Department of Physiology, Institute of Biomedicine, University of Turku, Turku, Finland.
Department of Pediatrics, Turku University Hospital, Turku, Finland.
Immunogenetics Laboratory, University of Turku and Turku University Hospital, Turku, Finland.
Department of Pediatrics, PEDEGO Research Unit, Medical Research Center, Oulu University Hospital and University of Oulu, Oulu, Finland.
Children's Hospital, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Research Programs Unit, Diabetes and Obesity, University of Helsinki, Helsinki, Finland.
Folkhälsan Research Center, Helsinki, Finland.
Tampere Center for Child Health Research, Tampere University Hospital, Tampere, Finland.
Fimlab Laboratories, Pirkanmaa Hospital District, Tampere, Finland.
Faculty of Veterinary Medicine, Department of Veterinary Biosciences, University of Helsinki, Finland.



Ljungan virus (LV) has not confirmed to associate with any human disease, but a possible connection with type 1 diabetes (T1D) has been suggested. Ljungan virus (LV) is a rodent-borne picornavirus that induces a diabetes-like condition in rodents. Approximately 30% of adults and 60% of children are seropositive in Finland. The Finnish Type 1 Diabetes Prediction and Prevention (DIPP) study enabled the use of very well characterized sample panels from children seroconverted to positivity for multiple islet autoantibodies during their prospective observation from birth, in addition samples from age, sex, HLA and residence area matched control children.


We analyzed LV IgG seroprevalence in 102 case children (65 had also developed T1D), in addition to non-diabetic control children. LV and human parechovirus (HPeV) immunofluorescence assays were used to analyze LV and HPeV specific IgG from 102 plasma samples taken at the time of islet autoantibody appearance, and from 204 samples from the matched control children.


Altogether 46.1% of the case and 50.7% of the control children were positive for LV IgG (odds ratio 0.8, 95% CI 0.47-1.36, p=0.416), and 67.6% vs. 79.8% were positive for HPeV IgG, respectively (odds ratio 0.49, 0.27-0.9, p=0.023).


Thus, no risk associations between LV or HPeV -specific IgG, and islet autoimmunity were observed. However, a trend for significantly higher prevalence of HPeV antibodies in control children (p=0.023) suggests a possible protective association of this virus with islet autoimmunity.

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