Scientists at Stanford Medicine have unveiled what they describe as a landmark finding in lupus research: the central role of the Epstein-Barr virus (EBV) in initiating the immune response that causes the condition. EBV, a member of the herpesvirus family, is highly common. By adulthood, about 95% of people worldwide carry it. The virus is transmitted through saliva or close personal contact, such as kissing or sharing drinks, and is well known for causing glandular fever when infection first occurs.
Science behind the discovery
Their study, published on 12 November 2025 in Science Translational Medicine, describes how EBV hijacks B cells and converts them into “driver” immune cells that recruit other immune components to attack the body’s own tissues. Until now, previous work had only hinted at EBV’s involvement in lupus. This new study maps out the mechanism in detail. “This is the single most impactful finding to emerge from my lab in my entire career,” said Professor William Robinson, Senior Author, Stanford Medicine. He emphasised that, in his view, the virus appears to underpin “100% of lupus cases”.
Lupus affects as many as five million people worldwide and is particularly prevalent among women. Its unpredictable symptoms and chronic organ involvement affecting the skin, joints, kidneys, heart, brain and other organs have long frustrated patients and clinicians alike.The new study showed that people with lupus had roughly one EBV-infected B cell for every 400 cells, whereas healthy controls had fewer than one EBV-infected B cell for every 10,000 cells. It also found that the virus preferentially infects autoreactive B cells, which already have the potential to target the body’s own tissues. This discovery helps explain how a virus that is typically silent in most people can trigger a relentless autoimmune attack.
Vaccine hopes and hurdles
With this breakthrough, attention may well shift toward vaccine development against EBV. Several early-stage programmes are already underway, including efforts by ModeX Therapeutics in partnership with Merck & Co., Grid Biosciences, EBViously and the US National Institutes of Health. However, none are yet close to market. As Prof Robinson cautioned: “That vaccine would have to be given soon after birth, and it would not be able to rid an already-infected person of the virus,” underscoring the complexity ahead.
New chapter for autoimmune research
Importantly, the Stanford team also suspects that the same mechanism – EBV infecting and reprogramming B cells – may extend beyond lupus to other autoimmune diseases such as multiple sclerosis, rheumatoid arthritis and Crohn’s disease. But they emphasise that their discovery is a scientific leap, not yet a solution. In Prof Robinson’s words: “Practically the only way to not get EBV is to live in a bubble.” As vaccine developers make sense of the news, the autoimmune sector could be at a pivotal moment. If EBV-based vaccines become viable, it could reshape not just lupus treatment but the broader landscape as a whole.
