A common childhood virus may be the hidden trigger behind lupus, a chronic autoimmune disease affecting millions worldwide, according to new research from Stanford University. The study, published this week in Science Translational Medicine, identifies the Epstein-Barr virus (EBV) as a key factor in the development of the disease.
New research from Stanford University links the Epstein-Barr virus to lupus disease, showing how the virus can push immune cells to attack the body’s own tissues.
“This is the single most impactful finding to emerge from my lab in my entire career,” said Dr. William Robinson, professor of immunology and rheumatology at Stanford and senior author of the study. “We think it applies to 100 per cent of lupus cases.”
Lupus causes the immune system to mistakenly attack healthy tissues, resulting in inflammation that can affect the skin, joints, kidneys, heart, and nervous system. Women are disproportionately affected, accounting for roughly 90 per cent of cases. While most patients manage symptoms with medication, including painkillers such as ibuprofen, around 5 per cent develop life-threatening complications. There is currently no cure.
Epstein-Barr virus is widely known for causing mononucleosis, or “mono,” often contracted in childhood or adolescence through saliva, such as by sharing food or drinks. Once inside the body, the virus remains in B cells, a type of immune cell responsible for producing antibodies.
Normally, B cells help defend the body, but EBV can hijack them. The virus convinces some cells to go rogue and persuade others to attack the body’s own tissues. This process, researchers found, appears to trigger lupus.
The Stanford team used advanced sequencing technology to study EBV’s effects on the immune system. They discovered that people with lupus have about 25 times more EBV-infected B cells than healthy individuals. The virus produces a protein called EBNA2, which activates human genes that drive inflammation. These rogue B cells then stimulate other immune cells to attack cell nuclei, a hallmark of lupus.
Robinson said similar viral mechanisms might contribute to other autoimmune disorders, including multiple sclerosis, rheumatoid arthritis, and Crohn’s disease. Factors such as genetics, viral strains, and environmental influences may explain why some people are more susceptible.
Several pharmaceutical companies are developing vaccines to prevent EBV infection, with some already in clinical trials. However, experts note that these vaccines would be most effective if administered early in life, before exposure to the virus.
The study offers a significant breakthrough in understanding lupus, potentially paving the way for new preventive strategies and therapies targeting the viral trigger.
