As per the recent study of Stanford Medicine, the Epstein-Barr virus (EBV) is a common human pathogen that can control the immune system and transform infected B cells into rogue commanders that trigger widespread autoimmune attacks. William Robinson and Dr. Shady Younis conducted research and published in Science Translational Medicine, which gives strong evidence that EBV is a direct cause of systemic lupus erythematosus (lupus). Robison claims that the process applies to all lupus cases and is referred to as the single most impactful finding of his career.
Lupus is a chronic autoimmune disease that affects up to 1 million Americans and 5 million people globally. This disease occurs when the immune system attacks the cell nuclei, damaging the skin, kidneys, joints, heart, and other organs. Symptoms may vary widely, and most patients can manage their disease with medication—about 5% face life-threatening complications. About 90% of patients are females, and it is not fully understood why this is so.
EBV infects around 95% of adults during childhood or adolescence through saliva. It can cause mononucleosis, but after the initial disease, the virus hides inside B cells. It is a type of white blood cell (WBC) that produces antibodies and activates other immune cells. EBV is a herpesvirus family and can remain dormant for years after introducing DNA into the nucleus of a host cell.
Most people coexist peacefully with latent EBV. Robinson’s team found that in lupus, the virus causes more B cells to play a destructive role. About 20% of B cells are autoreactive, capable of mistakenly targeting the body’s own tissues. These cells remain dormant, but when they are activated, they can produce antinuclear antibodies, which attack cell nuclei and trigger lupus.
Almost everyone with lupus has EBV, but for a long time, scientists have not been able to prove that the virus causes the disease. The Stanford research team solved this problem by producing a precise genetic sequencing method that can spot which B cells were infected with EBV. They found that in healthy people, about 1 out of 10,000 B cells carries the virus. People with lupus, 1 out of every 400 B cells is infected, which was a large elevation.
When EBV is asleep in the body, it sometimes makes a viral protein, EBNA2. This protein acts like a switch that turns on specific human genes inside an infected B cell. Some of those genes trigger even more genes that cause inflammation. These can lead to the activation of infected B cells and initiate the sending of signals to other immune cells known as helper T cells. They are already more likely to target their own body tissues.
Once these T cells are activated, they attract many self-reactive B cells and killer T cells, which create a large group of immune cells. They attack their own organs and tissues of the body. Most of these attacking cells are not infected with EBV; they are just misled and activated by a few infected cells, which set off the chain reaction.
These findings suggest that EBV reprogramming can contribute to the development of different autoimmune diseases like Crohn’s disease, rheumatoid arthritis, and multiple sclerosis. Though most people are infected with EBV, few develop autoimmunity, potentially because of specific viral strains. Many EBV vaccines are being developed, intended for early childhood administration. They cannot eliminate existing infections. Researchers co-founded EBVio Inc. to create a treatment that eliminates circulating B cells and allows the body to replace them with EBV-free cells from the bone marrow.
Reference: Goldman B. Stanford Medicine scientists tie lupus to a virus nearly all of us carry. Stanford Medicine News Center. November 12, 2025. Stanford Medicine scientists tie lupus to a virus nearly all of us carry
