Scientists believe they are closer to understanding how viruses might trigger type 1 diabetes and other autoimmune conditions.
A JDRF-funded study looked at the relationship between the Epstein-Barr virus, best known for causing glandular fever, and type 1 diabetes.
It is thought 90% of people will have contracted glandular fever by the time they reach the age of 20, and once they have it, it remains in the body forever.
Because the virus has been associated with other autoimmune conditions such as lupus, which inflames the joints and organs, American researchers from the Cincinnati Children’s Hospital Medical Center wanted to see why this link may exist.
The researchers focused their efforts on examining how the virus interacts with our DNA by using a specially developed computer programme.
The findings showed the Epstein-Barr virus produces a protein called EBNA2 which binds to several locations in the human genomen, which are linked with autoimmune conditions.
The results also show that viral or bacterial infections, poor diet, pollution or other environmental conditions might also impact human genes, which in turn might kick-start the development of autoimmune conditions.
Lead researcher Dr John Harley said: “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 diseases that don’t now exist.”
At the moment there is no vaccine currently available to prevent the EBV infection.
Leah Kottya, an immunobiology expert from the Center for Autoimmune Genomics and Etiology (CAGE) at Cincinnati, added: “I think we’ve come up with a really strong rationale for encouraging people to come up with more of an effort.
“Some EBV vaccines are under development. I think this study might well encourage them to push forward faster and with rededicated effort.”
The results have been published online in the journal Nature.

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