Stanford Medicine scientists tie lupus to a virus nearly all of us carry
Stanford researchers have finally uncovered the biological cause behind lupus, solving a decades-old mystery. Their new study, published in Science Translational Medicine on November 12, 2025, explains how a common virus can trigger this serious autoimmune condition.
Lupus, or systemic lupus erythematosus, affects more than 200,000 Americans. It occurs when the immune system mistakenly attacks healthy tissue, leading to fatigue, rashes, hair loss, and organ damage. The disease varies in severity and currently has no cure.
For years, scientists suspected the Epstein-Barr virus (EBV) played a role in lupus. EBV is extremely common—about 95% of adults carry it. It spreads mainly through saliva and usually causes mononucleosis. Once infected, the virus stays dormant for life.
Dr. William Robinson, professor of medicine and head of immunology and rheumatology at Stanford, led the study. He said that researchers had long been puzzled about why only a small number of people with EBV develop lupus.
To find the answer, Robinson’s team worked with experts from several institutions, including the University of Massachusetts School of Medicine, the U.S. Department of Veterans Affairs in Cincinnati, and the University of Oklahoma Health Sciences Center. They focused on how EBV interacts with B cells—white blood cells that produce antibodies.
B cells detect foreign substances called antigens. They then release antibodies to destroy them. In some cases, B cells become “autoreactive,” meaning they mistakenly attack the body’s own tissues. Normally, these cells remain inactive.
Robinson’s lab used advanced sequencing technology to track these cells. “We discovered that EBV infects the B cells responsible for autoimmunity and lupus,” Robinson said.
The study found that people with lupus had one in 400 B cells infected with EBV, compared to one in 10,000 in healthy individuals. Once inside, the virus can activate these cells, producing a viral protein called EBNA2. This protein triggers the immune system to attack healthy tissues, causing inflammation that harms the skin, kidneys, and joints.
“It not only infects autoreactive B cells but reprograms them into activated cells that drive autoimmunity,” Robinson explained.
The discovery opens new paths for treatment. Robinson and his co-authors have founded EBVio Inc., a startup focused on therapies that target infected B cells or reduce their numbers.
Experts say this could transform lupus care. Dr. Monica Gandhi, professor of medicine at UC San Francisco, called the study “exciting” because it provides a clear mechanism that could guide future treatments.
Dr. Narender Annapureddy of Vanderbilt University Medical Center added that over half of lupus patients do not respond well to existing therapies. He believes the findings could support newer treatments such as CAR-T cell therapy, which can reset the immune system and push patients into remission.
This research marks a major step forward in understanding and managing lupus—a condition that has long challenged medical science.
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