Now, the National Institutes of Health (NIH) are reporting another possible connection. Researchers at the Center for Autoimmune Genomics and Etiology at Cincinnati Children’s Hospital Medical Center have found a viral protein in EBV-infected cells. They think that the protein may turn on a “switch” that activates genes that are associated with an increased risk of autoimmune diseases. MS, of course, is an autoimmune disease.
Most people are infected with EBV. According to the Centers for Disease Control, it’s one of the most common human viruses. It usually appears in early childhood and its symptoms are generally very mild or don’t appear at all. But the EBV infection remains with people.
Scientists know that the EBV infection can produce a protein called EBNA2. In this new research, they found that EBNA2 activates some of the human genes associated with the risk of lupus and several other autoimmune diseases, including multiple sclerosis. Simply put, it flips that autoimmune disease “switch.”
“These findings suggest that EBV infection in cells can actually drive the activation of these genes and contribute to an individual’s risk of developing the disease,” said lead researcher John B. Harley, MD, PhD, in an NIH news release.
And that means more hope for new MS treatments and maybe even a cure.
Daniel Rotrosen, MD, director of the Division of Allergy, Immunology, and Transplantation at the National Institute of Allergy and Infectious Diseases, added that “now that we understand how EBV infection may contribute to autoimmune diseases in some people, researchers may be able to develop therapies that interrupt or reverse this process.”
Wouldn’t that be nice?
The journal Nature Genetics published the detailed research findings.
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