In a groundbreaking study, Stanford University researchers suggest that the extremely widespread Epstein-Barr virus (EBV) may play a critical role in triggering the autoimmune disease lupus. EBV affects more than ninety percent of people at some point in their lives and is most commonly known as the cause of infectious mononucleosis.
Lupus is an autoimmune disease in which the immune system attacks its own healthy tissue, leading to inflammation, pain and damage to organs such as the skin, joints, kidneys, heart and lungs. The disease is still a medical mystery, it has no clear cause and its symptoms often overlap with other diseases. There is not even a specific medicine aimed directly at its essence.
The Stanford researchers focused on how EBV affects B-lymphocytes, immune cells that normally help the body fight infections. Using advanced genetic analysis, they revealed that the virus reprograms these cells after infection. B-lymphocytes begin to function differently than they should, in a way that can confuse the immune system so much that it starts attacking its own tissues instead of harmful pathogens.
The key trigger turned out to be the viral protein EBNA2. According to research, this can start a chain reaction between immune cells that contributes to the development of lupus in individuals with a genetic predisposition. In a study published in the journal Science Translational Medicine, so the authors provide new insight into how EBV could initiate the disease in susceptible people.
