This virus infects almost everyone—and it may lead to lupus
Nearly all adults carry Epstein–Barr virus—but new research reveals how it can hijack immune cells, sparking a chronic disease that attacks the body from within.
For decades, scientists have suspected that a common virus most people acquire in childhood may later trigger lupus, a chronic autoimmune disease capable of damaging nearly every organ system in the body. But the precise link has remained unclear.
Now, new research from Stanford University offers one of the clearest explanations yet. The findings show how the Epstein-Barr virus (EBV) can hijack the body’s immune system in ways that may cause lupus in susceptible individuals.
“Globally, approximately 95 percent of adults have been infected with EBV, which means nearly all of us are carriers of this virus,” says William Robinson, a professor of immunology and rheumatology at Stanford and the senior author of the study.
EBV is known to take up long-term residence in the body’s B cells—immune cells responsible for producing antibodies. While it typically remains dormant after the initial infection, the study, published November 12 in Science Translational Medicine, reveals that EBV can sometimes reawaken and reprogram those cells, setting off the chain reaction that drives lupus.
Here’s what to know.
What is lupus—and why is it concerning?
Lupus, formally known as systemic lupus erythematosus, is a chronic autoimmune disease in which the immune system mistakenly attacks the body’s own organs and tissue. “It can affect joints, skin, kidneys, blood cells, and the brain,” Robinson says. An estimated 1.5 million Americans—and at least five million people worldwide—live with the condition, which disproportionately affects women.
(Why women are more prone to autoimmune diseases.)
Symptoms vary widely but often include fatigue, joint pain, swelling, and rashes. In more severe cases, the disease can inflame the kidneys, lungs, heart, or central nervous system.
“Lupus can lead to permanent organ damage, disability, and even an increased risk of early death,” says Shady Younis, an immunologist and rheumatologist at Stanford University and the study’s lead author.
Inside the new research
Despite decades of research, scientists still don’t fully understand what triggers lupus or how genetic risk and environmental factors, including viral infections, interact.
To clarify EBV’s role in the development of the disease, Robinson and his team collected blood samples from 11 people with lupus and 10 healthy volunteers. Using a specialized single-cell sequencing method they developed, the researchers analyzed the full genetic material of more than 300,000 individual B cells to determine which ones carried the virus.
The new method made it possible to spot rare infected cells hidden among vast numbers of healthy ones—something earlier techniques couldn’t do. The team then quantified the infected cells, examined which subsets EBV targeted, and observed how the virus altered them.
The results were striking: EBV-infected B cells were about 25 times more common in people with lupus than in the healthy individuals. Even more revealing, EBV showed a strong preference for infecting “autoreactive” B cells—the very ones most likely to target the body’s own tissues mistakenly. “It was targeting and empowering exactly the B cells that drive lupus,” says Younis.
Once inside these cells, EBV appeared to switch on viral genes and immune pathways associated with chronic inflammation and autoimmunity, essentially turning autoreactive B cells into hubs that amplify lupus activity.
The findings offer one of the strongest mechanistic explanations yet for how “a very common virus may be contributing to a relatively uncommon but devastating autoimmune disease,” says Younis.
Deepak Rao, a rheumatologist and immunologist at Brigham and Women’s Hospital in Massachusetts, who was not involved in the research, says the paper “does a beautiful job of outlining a potential mechanistic connection” between EBV-infected B cells and lupus, highlighting immune pathways scientists couldn’t previously track.
Still, the study does have limitations. The team primarily examined B cells circulating in the blood rather than those residing in organs such as the kidneys—organs where lupus often causes its most severe damage. And while the findings strongly support a causal role for EBV-infected autoreactive B cells, Robinson emphasizes that more research is needed to understand why only some EBV carriers develop lupus while others do not, and how genetic or environmental factors may further shape risk.
(Chronic kidney disease is on the rise—and many people don’t know that they have it.)
Where the science goes from here
Beyond solving a long-standing mystery, the findings point to new possibilities for prevention, diagnosis, and treatment.
On the prevention front, “our findings strengthen the case for EBV vaccines and antiviral strategies as potential tools to prevent not only EBV infections but also EBV-related autoimmune disease,” Robinson says. This matters because several EBV vaccines are already in early clinical trials, raising the possibility that protecting against the virus could one day help reduce lupus risk.
The work may also sharpen diagnosis. Detecting EBV-infected autoreactive B cells, or the molecular traces they leave behind, could help identify people at higher risk or clarify what’s driving an individual patient’s disease.
(How pig transplants are giving hope to kidney disease patients.)
But perhaps the most exciting implications lie in treatment. “The study points to new therapeutic strategies that selectively target EBV-infected B cells, using approaches such as engineered T cells or bispecific antibodies while sparing healthy immune cells,” Younis says. These targeted treatments could complement or even surpass existing treatments, many of which broadly suppress the immune system rather than correcting the malfunction at its source.
“The goal now,” Robinson notes, “is to turn these biological insights into more precise, durable, and potentially curative therapies for people living with lupus.”
