Researchers have gained insight from a new study into how environmental factors such as viruses could contribute to the development of type 1 diabetes (T1D) and other autoimmune conditions. The study found that a protein produced by a virus binds to different genes associated with seven autoimmune conditions including T1D.
Only about 5% of people with T1D risk genes go on to develop the disease. While we do not know exactly what causes T1D, researchers have established it is a combination of genetics and environmental factors. Something in the environment is ‘switching on’ T1D genes in certain people. Viruses are one of many environmental factors under investigation for their role in T1D.
The researchers involved in this study work on the autoimmune disease lupus, where the immune system attacks skin, joints and other organs. They wanted to find out more about the links between lupus and one particular virus called Epstein Barr Virus (EBV). EBV is infamous for causing glandular fever, which affects 90% of people by the time they are 20. The EBV infects immune cells, and once infected, stays in the body for life.
The team developed a computer program to help them analyse existing genetic datasets and spot if the viral proteins bind in areas of the genome known to increase the risk for lupus, and they also investigated genes associated with other autoimmune conditions.
They found that the EPV produces a protein called EBNA2, and this EBNA2 protein was bound to genes associated with risk for lupus as well as T1D, multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, juvenile idiopathic arthritis and coeliac disease. EBNA2 was found associated with other proteins called transcription factors, which together changes how genes are controlled.
These findings indicate a possible mechanism for how exactly a virus, combined with genetic predisposition, could lead to the development of an autoimmune condition like T1D.
If certain viruses do trigger T1D, it is unlikely to be the whole picture. For example, they may only trigger T1D in people with one specific gene pattern, or, T1D may be triggered by a combination of environmental factors building up, such as viruses, gut bacteria and particular nutrients. We don’t know this yet.
Next, the research team are going to share the software they developed and make all of their data and results publicly available, which means researchers all over the world including T1D researchers can use the data to further their own research towards prevention of T1D and other autoimmune diseases.
What’s happening in Australia ?
There is some exciting JDRF-funded research in the environmental factors and prevention area in Australia. A few key projects across different states are broadening our understanding of the environmental factors linked to T1D.
In NSW, Professor Maria Craig and her team are mapping out all viruses known to infect humans, to see which ones are definitively linked to T1D. Then, this information can be used to develop a vaccine.
The ENDIA study led by Professor Jenny Couper in SA is collecting information on a whole host of environmental factors such as viruses, bacteria, nutrition and growth in early life to find out which cause or protect against T1D. You can get involved in this study if you are expecting or have recently had a baby that will have a first-degree relative with T1D (mum, dad, sibling). To find out more head to their website.
Different teams across the country are specifically investigating gut bacteria links with T1D, including Future Research Leaders Dr Emma Hamilton-Williams in QLD and Dr Eliana Marino in VIC (FRLP) as well as senior researcher Prof Len Harrison in VIC.
A common mechanism?
This research highlights how there might be a common mechanism between T1D and some autoimmune diseases – did you know that 25% of people with T1D also have one or more other autoimmune disease? That means that research taking place for other autoimmune diseases could one day benefit people with T1D, and the research we fund into T1D could benefit the 5% of Australians living with an autoimmune disease.