JDRF-funded researchers at the University of Cambridge have found evidence of a link between viral infection and the development of type 1 diabetes.
They discovered that a genetic response normally associated with infection preceded the first indications of the condition in children.
“We can now move our research forward to dissect out what effects such an anti-viral gene response has on the immune system to increase the risk of autoimmunity and type 1 diabetes in very young children,” commented Professor John Todd, Director of the JDRF/Wellcome Trust Diabetes and Inflammation Laboratory at the Cambridge Institute for Medical Research, a co-director of the project.
He and JDRF postdoctoral fellow Dr Ricardo Ferreira, who led the research, believe their findings could lead to a way of identifying children at increased risk of type 1, even before they develop the immune system proteins, known as autoantibodies, that are currently the only immune system marker for the condition before symptoms arise.
Scientists have long known that there is a strong genetic element to being at increased risk of type 1. But not everyone with this increased inherited risk goes on to develop the condition. Research suggests that environmental factors must be important but their identities largely remain elusive, with viral infections being the lead candidate. Last year, JDRF-funded research in Finland pointed to the coxsackie B virus as one potential environmental trigger.
The Cambridge research lends support to this idea. The genes identified are usually activated when the body produces a protein called type I interferon, which is emitted by cells when they encounter a virus.
Among children suspected to be at high risk of developing type 1 diabetes, these genes were most strongly activated, or ‘expressed’, in those who subsequently went on to produce autoantibodies to pancreatic cells, whereas children who did not develop this immune response during the study had lower levels of activation.
In contrast, the genes were only weakly expressed in healthy participants and people who already had type 1 diabetes. This suggests that the response is limited to the period before the immune response is triggered, and could therefore lead to a way of identifying who is at greatest risk of developing the condition, allowing them to access treatment earlier than is currently possible.
Ferreira said: “We now have a handle on a potential biomarker that can be detected easily in a tiny blood sample that may indicate viral infections with predisposing effects in autoimmunity against the insulin-producing cells of the pancreas.”
The researchers also found a link to respiratory infections, as children who had a recent respiratory condition were more likely to have the high level of gene activation.
However, because the illness data was self-reported by parents, there was no record of which infections these were, beyond being respiratory tract infections. The researchers now hope to carry out a study with additional infection data, potentially allowing them to track the effects of viruses on type 1. The JDRF-funded TEDDY study, which is recording the infections, allergies and diets experienced by young people at risk of developing the condition, is one source they hope to use.
Karen Addington, Chief Executive of JDRF, said: “The results of this study certainly appear worthy of being explored further. Type 1 diabetes is a challenging and complex condition. But it will one day be cured. It's just a matter of time, money and excellent research such as this.”
The study, funded by JDRF, the type 1 diabetes charity, and the Wellcome Trust, was published today in the journal Diabetes.