A new animation from the ENT1DEP consortium explains the growing evidence linking common viruses to type 1 diabetes, and the prevention research this evidence has opened up.
Why are researchers looking at viruses?
T1D is partly influenced by genetic factors. However, 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 illnesses. Even in the absence of severe symptoms the virus can enter the blood and spread to organs which are susceptible for the virus. Pancreas is once such organ, and beta-cells may be particularly susceptible since they express high amounts of molecules which the virus needs to enter the cell.
Interestingly, both enteroviral genetic material and live replicating viruses have been detected in pancreatic tissue from T1D patients, whereas viral presence has been clearly less common in healthy controls. Evidence of enterovirus infection has now 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.
Diagram of pancreatic islet, showing insulin-producing beta cells and surrounding acini cells © Oslo University Hospital, 2026
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 video presented here, 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 – altered molecules that the immune system may recognize as “non self”. This can initiate an autoimmune response, leading to the production of autoantibodies and ultimately, an immune-mediated attack of beta cells.
Early antiviral treatment and vaccines as potential prevention strategies
The growing number of studies supporting the enterovirus hypothesis has opened new possibilities for intervention and prevention. A recent clinical study tested the effect of antiviral treatment in children newly diagnosed with type 1 diabetes. The trial showed that treatment significantly preserved residual insulin production, suggesting reduced beta cell damage caused by viruses. The researchers behind the study are now planning to test intervention with antiviral drugs at an earlier stage of disease development, with the aim of preserving more beta cells. Read more about the study→ Pleconaril and ribavirin in new-onset type 1 diabetes: a phase 2 randomized trial.
In addition, an enterovirus vaccine developed in Finland has recently been tested in humans, showing good safety and a promising immune response. This development holds great potential for future vaccination strategies aimed at preventing type 1 diabetes in children. More information is available in the study→ Safety and immunogenicity of a vaccine against Coxsackieviruses B (PRV-101).
ENT1DEP is an EU-funded research consortium bringing together several distinguished research groups to advance this mission. This video has been created to help stakeholders and the scientific community follow the consortium’s work, while also raising awareness of the major medical and socioeconomic importance of efforts to prevent type 1 diabetes.
Scientific Production Group
The scientific content was developed by an international Scientific Production Group comprising leading experts in virology, immunology, cell biology, and clinical diabetology.
Oslo, Norway
Tampere, Finland
Paris, France
Exeter, UK
Animation Production
Produced by XVIVO Scientific Animation (Connecticut, USA).