A Virus Almost Everyone Carries Could Finally Explain What Causes Lupus

New research reveals how Epstein-Barr virus can turn the immune system against the body itself.

For more than half a century, scientists have hunted for the cause of lupus. The disease is relentless and debilitating, one that turns the immune system against the very body it’s meant to protect. It can inflame joints, skin, kidneys, even the brain. And while its symptoms have been mapped in painful detail, its origin has remained a riddle.

Now, researchers at Stanford University believe they’ve solved it. The culprit isn’t a mysterious toxin or a rare mutation — it’s a childhood virus nearly everyone carries.

The Epstein-Barr virus (EBV), best known for causing mononucleosis, may be the long-suspected spark behind lupus, according to new findings published in Science Translational Medicine.

“This is the single most impactful finding to emerge from my lab in my entire career,” said William Robinson, professor of immunology and rheumatology at Stanford University and senior author of the study.

“We think it applies to 100% of lupus cases.”

The Virus That Lives Inside Us

EBV is a member of the herpesvirus family, the same group responsible for chickenpox and cold sores. It spreads easily through saliva, typically in childhood or adolescence, which is why almost everyone has it. Once infected, you carry the virus for life.

“Practically the only way to not get EBV is to live in a bubble,” Robinson said.

The virus hides in B cells, the immune system’s antibody factories. In healthy people, these cells patrol for pathogens. But about 20% of them are “autoreactive,” meaning they’re capable of targeting the body’s own tissues. Normally, that almost never happens.

The Stanford study shows how EBV hijacks that system. It slips into these autoreactive B cells and reprograms them. Using a cutting-edge single-cell sequencing method, Robinson’s team examined hundreds of thousands of B cells from lupus patients and healthy controls. The results were stark: lupus patients had 25 times more EBV-infected B cells — about one in every 400 — compared to one in 10,000 in healthy individuals.

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“We think this is the critical discovery: that EBV … then activates those B cells to drive the autoimmune response that mediates lupus,” Robinson told The Guardian.

When EBV activates within those cells, it produces a protein called EBNA2, which acts as a genetic switch. That switch turns on inflammatory genes, transforming sleepy autoreactive B cells into aggressive ones. These rogue cells churn out autoantibodies—the self-targeting missiles that define lupus—and recruit other immune cells into battle.

The cascade becomes self-perpetuating. What begins as a viral hack inside a few cells ends as an immune uprising across the body.

Why Some People Get Lupus — But Most Don’t

If EBV infects nearly everyone, why do only some people develop lupus? The answer, for now, is unclear.

Robinson suspects viral strain differences or genetic susceptibility play a role. Hormones may also shape vulnerability: about nine out of ten lupus patients are women, and estrogen may amplify B-cell activity. People of African, Caribbean, or Asian ancestry face higher risks.

The team also acknowledges that some medications used to treat lupus might make it easier for EBV to replicate, complicating the picture. Still, the study provides one of the strongest mechanistic links yet between EBV and autoimmune disease.

Deepak Rao, a rheumatologist at Brigham and Women’s Hospital, called it “a beautiful job of outlining a potential mechanistic connection.”

Toward a Future Without Lupus

For the millions living with lupus, the new findings could open a path toward more precise treatments. Current therapies work by broadly suppressing the immune system. This reduces the painful lupus symptoms but leaves patients vulnerable to infection.

“I think it really sets the stage for a new generation of therapies that could fundamentally treat and thereby provide benefit to lupus patients,” Robinson said.

Next-generation approaches might instead target EBV-infected B cells specifically, using engineered T cells or bispecific antibodies that leave healthy immune cells untouched. Meanwhile, several EBV vaccines are already in clinical trials. If they work, they could prevent not only mononucleosis but possibly lupus and other EBV-linked diseases such as multiple sclerosis and some cancers.

“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 told National Geographic.

A virus most of us caught from a childhood kiss or a shared spoon might hold the key to one of medicine’s oldest puzzles. The mystery of lupus, once thought unsolvable, is starting to come into focus — and the solution may lie hidden inside nearly every human cell.

“The goal now,” Robinson said, “is to turn these biological insights into more precise, durable, and potentially curative therapies for people living with lupus.”