Infection with Epstein-Barr virus has been associated with the development chronic autoimmune illnesses, but the mechanisms behind this association have been unclear. Scientists supported by the National Institute of Allergy and Infectious Diseases said that a novel computational method shows that a viral protein found in EBV-infected human cells may activate genes associated with increased risk for autoimmunity. 

When EBV infects human immune cells, a protein produced by the virus –  EBNA2 – recruits human proteins called transcription factors to bind to regions of both the EBV genome and the cell's own genome. Together, EBNA2 and the human transcription factors change the expression of neighboring viral genes.

In the current study, the researchers found that EBNA2 and its related transcription factors activate some of the human genes associated with the risk for multiple sclerosis. The investigators used Regulatory Element Locus Intersection algorithm, or RELI, to probe regulatory genes associated with autoimmune diseases and found that EBNA2 bound to genes associated with the risk for MS.

Researchers note that EBV infection is not the only factor that contributes to the development of the seven autoimmune conditions discussed in the paper. Many of the regulatory genes that contribute to autoimmune disorders did not interact with EBNA2, and some individuals with activated regulatory genes associated with disease risk do not develop disease.

EBV infection is nearly ubiquitous in the human population worldwide. Most people acquire EBV in early childhood, experience no symptoms or only a brief, mild cold-like illness, and remain infected throughout their lives while remaining asymptomatic. 

The findings were published in Nature Genetics.