A growing body of research suggests that viral DNA or proteins introduced into the body can contribute toward the development of serious diseases long after the initial viral infection has passed.
Now, a groundbreaking study by a team from the Cincinnati Children’s Hospital shows that exposure to the Epstein-Barr virus (EBV), best known for causing mononucleosis, appears to boost the risk of developing seven other diseases in individuals who inherited predisposing gene variants. Those autoimmune diseases are lupus, multiple sclerosis, rheumatoid arthritis, juvenile idiopathic arthritis, inflammatory bowel disease, celiac disease, and type 1 diabetes.
The paper, published in Nature Genetics, sheds light on how diseases with complex origins may arise and provides molecular targets for future treatments.
EBV is so prevalent that an estimated 90 percent of individuals will be infected by the time they are 20. Once inside the body, the virus inserts a copy of its genome into B cells, instructing the cell to produce its viral proteins for it. When the B cell replicates and divides, so does the viral genome, and thus, the virus and its protein products linger in the body indefinitely.
The seven diseases are known to arise after B cells mistakenly flag the body’s own tissue as dangerous, yet a combination of environmental and genetic factors appear to be at play.
To connect the dots between EBV, B cells, genetics, and the development of autoimmune disease, a team co-led by Dr John Harley analyzed a large database of DNA sequences from EBV-infected and EBV-negative B cells using an algorithm that identifies regions where proteins that may influence gene transcription are bound to the strand.