How viruses may cause type 1 diabetes. A hope for prevention
Type 1 diabetes (T1D) is a chronic disease in which the immune system destroys the insulin-producing beta cells in the pancreas. Without these cells, the body cannot regulate blood sugar on its own. People with T1D need insulin therapy every day for the rest of their lives.
Nearly 10 million people live with T1D worldwide, and this number is predicted to double in 20 years. The disease is serious not only because of the long-term complications it can cause, but also because managing it places a substantial daily burden on patients and their families. There is an urgent need for new treatment and prevention strategies.
Why are researchers looking at viruses?
T1D is partly influenced by genetic factors. But genetic susceptibility alone cannot explain the rapidly increasing incidence of T1D worldwide. This has led researchers to investigate environmental factors that may trigger or accelerate the autoimmune process. Among the most studied candidates are viral infections, particularly enteroviruses such as Coxsackie B viruses. A growing number of studies suggest that these viruses may play a key role in triggering T1D in genetically susceptible individuals.
Enteroviruses are common and usually cause mild illness. Even in the absence of severe symptoms, the virus can enter the bloodstream and spread to organs that are susceptible to infection. The pancreas is one such organ, and beta cells may be particularly vulnerable because they express high amounts of molecules that the virus uses to enter cells. Researchers have detected both enteroviral genetic material and live replicating viruses in pancreatic tissue from people with T1D, while viral presence has been less common in healthy individuals. Evidence of enterovirus infection has been observed in both the early and later stages of the disease, strengthening the hypothesis that these viruses may contribute to the initiation and progression of T1D.
How could a virus trigger type 1 diabetes?
By combining findings from studies investigating the link between enteroviruses and T1D, researchers have proposed a model describing how viral infection may lead to destruction of insulin-producing beta cells and eventually trigger autoimmune T1D. The model illustrated in the animation begins with viruses entering beta cells in the pancreas and establishing a low-grade, persistent infection.
As the viruses slowly replicate over time, they induce cellular stress and promote the formation of misfolded proteins and neoantigens which are altered molecules that the immune system may recognise as “non-self”. This can initiate an autoimmune response, leading to the production of autoantibodies and ultimately an immune-mediated attack on beta cells. Over time, enough beta cells are destroyed that the person develops type 1 diabetes.
Early antiviral treatment and vaccines: potential prevention strategies
The growing evidence supporting the enterovirus hypothesis has opened new possibilities for intervention and prevention.
A recent clinical study tested the effect of antiviral treatment in newly diagnosed children with T1D. The trial showed that the treatment significantly preserved residual insulin production, indicating reduced beta cell death caused by the viruses. Researchers are now planning to test antiviral treatment at an earlier stage of disease development, to potentially save more beta cells. Read More→
An enterovirus vaccine developed in Finland has recently been tested in humans for the first time, showing good safety and an immunogenic effect. This holds great potential for future vaccination of children to prevent T1D. Read More→
Supporting Awarness and Prevention Research
Scientific production group
The scientific content were developed by an international Scientific Production Group comprising leading experts in virology, immunology, cell biology, and clinical diabetology.
| Knut Dahl-Jørgensen | Heikki Hyöty | Roberto Mallone | Sarah Richardson |
|---|---|---|---|
| Oslo University Hospital, Norway | Tampere University, Finland | Université Paris Cité / INSERM, France | University of Exeter, UK |
Animation Production
Animation produced by XVIVO Scientific Animation (Connecticut, USA).
Funding Acknowledgement
This project has received funding from the European Union’s Horizon Europe research and innovation programme under Grant Agreement No. 101137457.
Copyright
© Oslo University Hospital, 2026