On Nov. 12, 2025, Stanford Medicine scientists have found that the Epstein-Barr virus can convert B cells it’s infected into diabolical overlords that reprogram myriad other immune cells to attack our tissues. One of humanity’s most ubiquitous infectious pathogens bears the blame for the chronic autoimmune condition called systemic lupus erythematosus or, colloquially, lupus, Stanford Medicine investigators and their colleagues have found.

The Epstein-Barr virus (EBV), which resides silently inside the bodies of 19 out of 20 Americans, is directly responsible for commandeering what starts out as a minuscule number of immune cells to go rogue and persuade far more of their fellow immune cells to launch a widespread assault on the body’s tissues, the scientists have shown.

Several hundred thousand Americans (by some estimates close to a million) and about 5 million worldwide have lupus, in which the immune system attacks the contents of cell nuclei. This results in damage to organs and tissues throughout the body — skin, joints, kidneys, heart, nerves and elsewhere — with symptoms varying widely among individuals. For unknown reasons, nine out of 10 lupus patients are women.

With appropriate diagnosis and medication, most lupus patients can live reasonably normal lives, but for about 5% of them the disorder can be life-threatening, said William Robinson, MD, PhD, who is the James W. Raitt, MD, Professor. Existing treatments slow down disease progression but don’t cure it, he said.

By the time we’ve reached adulthood, the vast majority of us have been infected by EBV. Transmitted in saliva, EBV infection typically occurs in childhood, from sharing a spoon with or drinking from the same glass as a sibling or a friend, or maybe during our teen years, from exchanging a kiss. EBV can cause mononucleosis, “the kissing disease,” which begins with a fever that subsides but lapses into a profound fatigue that can persist for months.

The million-dollar question: If about 95% of us are walking around with latent EBV in our B cells, why do some of us, but not all of us, get autoimmunity? Robinson speculates that perhaps only certain EBV strains spur the transformation of infected B cells into antigen-presenting “driver” cells that broadly activate huge numbers of antinuclear B cells.

Many companies are working on an EBV vaccine, and clinical trials of such a vaccine are underway. But that vaccine would have to be given soon after birth, Robinson noted, as such vaccines are unable to rid an already-infected person of the virus. The findings were published in Science Translational Medicine.