In a medical breakthrough that could revolutionise treatment approaches, scientists have confirmed that the near-ubiquitous Epstein-Barr virus (EBV) serves as the primary trigger for the autoimmune condition lupus.
The groundbreaking research from Stanford University reveals how this common childhood infection, carried by approximately 95% of adults, can cause immune cells to go rogue and mistakenly attack the body's own tissues.
The Cellular Mechanism Uncovered
The study, published in Science Translational Medicine, provides the first cellular-level explanation for how EBV sends the immune system into a tailspin. Using high-precision genetic sequencing, researchers compared B cells in 11 lupus patients against 10 healthy controls.
The findings were striking: lupus patients showed EBV presence in about 1 in 400 B cells, compared to fewer than 1 in 10,000 cells in healthy individuals - representing a 25-fold difference.
Professor William Robinson, the study's senior author and a professor of immunology and rheumatology at Stanford, stated unequivocally: "We think it applies to 100% of lupus cases. I think it really sets the stage for a new generation of therapies that could fundamentally treat and thereby provide benefit to lupus patients."
How a Common Virus Triggers Autoimmunity
EBV typically causes mild childhood illness with symptoms like sore throat, fever and tonsillitis. Most people contract it during childhood or adolescence and carry the dormant virus in their cells throughout life.
The research team discovered that EBV takes up permanent residence in B cells, which are crucial components of the immune system. About 20% of B cells naturally have the potential to bind to the body's own tissues, but in healthy individuals, these autoreactive B cells remain largely inactive.
However, in lupus patients, the presence of dormant EBV flips these cells into a hyperactive state. They not only target the body's own antigens but also recruit other immune cells, including killer T-cells, to join the attack.
"We think this is the critical discovery: that EBV then activates those B cells to drive the autoimmune response that mediates lupus," Professor Robinson explained.
Broader Implications and Future Treatments
The findings resolve what first author Shady Younis described as "a decades-old mystery" in autoimmune research. The connection gains additional significance following recent breakthroughs proving EBV's link to multiple sclerosis, another autoimmune disorder.
Lupus affects approximately 69,000 people in the UK, with the condition causing joint and muscle pain, extreme tiredness and skin rashes. The disease disproportionately affects women and shows higher prevalence among people of African, Caribbean or Asian background.
Professor Guy Gorochov of Sorbonne University, who was not involved in the research, described the work as "impressive", adding that while it's not the final paper on lupus, the team had "developed an interesting concept."
The confirmation of EBV's role adds significant impetus to ongoing clinical trials for an EBV vaccine. Researchers are also exploring repurposing cancer treatments designed to wipe out B cells for severe lupus cases.
As Professor Robinson noted, the virus's ubiquity makes prevention challenging: "Practically the only way to not get EBV is to live in a bubble." This reality makes the pursuit of effective vaccines and targeted treatments even more critical for the thousands living with this chronic condition.
