Epstein-Barr ‘Switches On” Autoimmune Genes

New research suggests an Epstein-Barr virus protein can ignite risk genes for autoimmune diseases.


The Epstein-Barr virus (EBV) protein can “switch on” risk genes for autoimmune diseases, according to researchers from the National Institute of Allergy and Infectious Diseases. They found that when EBV infects human immune cells, the virus produces a protein (EBNA2) that “recruits” human proteins (transcription factors) to bind to regions of both the EBV genome and the cell’s own genome. Together the viral protein and the human transcription factors change the expression of neighboring viral genes.

In the study, EBNA2 and its related transcription factors activated some of the genes associated with the risk for lupus, multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, type 1 diabetes, juvenile idiopathic arthritis, and celiac disease.

Previous research had also suggested that EBV infection plays a role in autoimmune diseases, particularly lupus. The researchers in the current study speculated that genetic analysis could further explain the relationship. They used a new computational and biochemical technique to sift through genetic and protein data, looking for potential regulatory regions in genes associated with the risk of developing lupus that also bound to EBNA2 and its transcription factors.

“We were surprised to see that nearly half of the locations on the human genome known to contribute to lupus risk were also binding sites for EBNA2,” said John Harley, MD, PhD, lead investigator.

The researchers caution, however, that many of the regulatory genes that contribute to lupus and other autoimmune disorders did not interact with EBNA2, and some individuals with activated regulatory genes do not develop disease.

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