Due to copyright issues, an electronic copy of the thesis must be ordered from the faculty. For the faculty to have time to process the order, the order must be received by the faculty at the latest 2 days before the public defence. Orders received later than 2 days before the defence will not be processed. After the public defence, please address any inquiries regarding the thesis to the candidate.
Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Professor Michael J. Haller, University of Florida, USA
- Second opponent: Professor Helena Elding Larsson, Lund University, Sweden
- Third member and chair of the evaluation committee: Professor Ketil Størdal, University of Oslo
Chair of the Defence
Professor Kåre Inge Birkeland, University of Oslo
Principal Supervisor
Senior Consultant Lars Krogvold, Oslo University Hospital
Summary
Type 1 diabetes is an autoimmune disease in which genetic susceptibility and environmental factors contribute to immune-mediated destruction of insulin-producing β-cells. Increasing evidence suggests that enteroviruses may contribute to disease development. This thesis investigated the role of viral infections in type I diabetes through analyses of pancreatic tissue and a randomized controlled trial.
Pancreatic biopsies from living adults newly diagnosed with type 1 diabetes showed signs of persistent viral activity and cellular stress. RNA analyses and immunohistochemistry demonstrated upregulation of pathways associated with viral replication, ongoing infection and cellular stress, and increased expression of antiviral markers, indicating an ongoing antiviral response in the pancreas.
A randomized, double-blind clinical trial including 96 children and adolescents newly diagnosed with type 1 diabetes was conducted. They were treated with pleconaril and ribavirin or placebo for six months. Antiviral treatment slowed the decline in endogenous insulin production during the first year after diagnosis, although the effect was not sustained long term.
Overall, the findings support the hypothesis that persistent low-grade viral infections contribute to type 1 diabetes pathogenesis. They also provide a foundation for further research into antiviral treatment strategies, both for type 1 diabetes but also for other autoimmune diseases.
Additional information
Contact the research support staff.