Could glandular fever trigger type 1 diabetes and other autoimmune conditions?

Posted on 27 April 2018

Young woman lying ill with a mug

Scientists believe they may have moved closer to understanding how exactly a virus could trigger type 1 diabetes and other autoimmune conditions.

A recent study found that a protein produced by a virus binds to multiple sections of the human genome associated with seven autoimmune conditions, including type 1 diabetes.

The Epstein-Barr virus, most famous for causing glandular fever, infects immune cells. The virus produces a protein which can then bind to specific sections of DNA, and lead to changes in how certain genes are controlled.

The findings from this work offer a suggestion of how exactly an environmental factor, like a virus, could be triggering autoimmune conditions.

Why did they do this research?

The Epstein-Barr virus is very common, and 90 per cent of people will catch it by the time they are 20. Once infected, the virus stays in the body for life.

Over the years, the virus has been linked with a number of conditions, including lupus, an autoimmune condition that leads to inflammation in the joints, skin and other organs.

A team of researchers from the USA therefore decided to investigate how the Epstein-Barr virus was interacting with the DNA in our genome, and whether the protein produced by the virus was binding to regions associated with a higher risk of lupus, and other autoimmune conditions including type 1 diabetes.

What did they do?

The team developed a computer program to help them analyse existing genetic datasets and spot if the virus protein binds in areas of our genome that we know increase the risk for different autoimmune conditions.

The computer program also checked whether ‘controller’ proteins bind in these areas. These controller proteins work to regulate genes and switch them on and off.

What did they find?

The virus protein binds to sections of the human genome which we know increase the risk of type 1 diabetes, multiple sclerosis (MS), lupus, and coeliac disease, amongst others, along with a number of controller proteins.

Further analysis suggested that this may then change the way certain genes are controlled.

What does this mean for type 1?

We’ve known for many years that having certain genes can increase a person’s risk of developing type 1 diabetes. What remains unclear however is how exactly type 1 diabetes can be triggered in people with these genes.

Scientists have long suspected viruses of playing a role in triggering type 1 diabetes, at least in some cases. These findings now indicate a possible mechanism for how exactly a virus, combined with the genetic predisposition, could lead to the development of an autoimmune condition like type 1 diabetes.

Lead researcher on the study, Dr John Harley, said of the findings:

“This discovery is probably fundamental enough that it will spur many other scientists around the world to reconsider this virus in these disorders.”

“As a consequence, and assuming that others can replicate our findings, that could lead to therapies, ways of prevention, and ways of anticipating disease that don’t now exist.”

What’s the next step?

The team will be sharing the software they developed as part of this project, and make all of their data and results publicly available. The researchers have also started contacting experts on different conditions to see if they would be interested in collaborating and investigating these findings further.

JDRF is partnering with other autoimmune disease charities Arthritis Research UK and MS Society to drive the Connect Immune Research initiative which we hope will enable more scientists to understand more about how different autoimmune conditions may be linked – and therefore how we could tackle them together.

Type 1 diabetes research in a laboratory

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