Almost everyone carries it. The Epstein-Barr virus, best known as the cause of infectious mononucleosis, infects the vast majority of people at some point in life, usually with such mild or unnoticeable symptoms that most never realize they were exposed. For decades that near-universal infection seemed largely benign once the initial illness passed. But a growing body of evidence now points to Epstein-Barr virus as a leading suspect in the development of multiple sclerosis, a disabling disease of the central nervous system.
The idea that a common childhood virus could set the stage for a serious autoimmune disease has reshaped how scientists think about multiple sclerosis. A landmark study of millions of young adults found that infection with the virus dramatically raised the later risk of the disease, strengthening the case that the two are causally linked rather than merely associated. The findings have energized efforts to prevent or treat the virus as a possible route to preventing multiple sclerosis itself.
A virus nearly everyone eventually carries
Epstein-Barr virus is a member of the herpesvirus family and one of the most widespread human viruses. As its virology describes, it spreads mainly through saliva, which is why it earned the nickname the kissing disease, and it establishes a lifelong latent infection in certain immune cells after the initial exposure. In young children the first infection often causes little more than a mild cold; in adolescents and adults it more frequently produces the fever, sore throat, and exhaustion of mononucleosis.
Once inside the body, the virus never fully leaves. It persists quietly in B cells, the immune cells that produce antibodies, and can periodically reactivate. That lifelong presence, combined with its ability to manipulate the immune system, has long made it a candidate for a role in diseases far removed from the sore throat it first causes.
What multiple sclerosis does to the nervous system
Multiple sclerosis is a chronic disease in which the immune system attacks myelin, the fatty insulation that wraps around nerve fibers in the brain and spinal cord. As that insulation is damaged, the electrical signals traveling along nerves slow or fail, producing symptoms that can include numbness, weakness, vision problems, difficulty walking, and fatigue. The disease typically strikes young adults and follows an unpredictable course, sometimes relapsing and remitting, sometimes steadily progressing.
The cause of multiple sclerosis has never been fully explained. Genetics, low vitamin D, smoking, and geography all appear to influence risk, but none accounts for the disease on its own. That gap is what made the search for an infectious trigger so compelling, and what made the Epstein-Barr findings so significant.
The 20-year study that changed the picture
The strongest evidence came from a study tracking more than 10 million young adults on active duty in the U.S. military over roughly two decades. Because the military stores blood samples collected periodically, researchers could compare each person’s Epstein-Barr status before and after some developed multiple sclerosis. The analysis published in the journal Science in 2022 found that infection with the virus raised the risk of subsequently developing multiple sclerosis roughly 32-fold.
Crucially, that jump in risk was not seen after infection with other viruses transmitted in similar ways, which argues against the finding being a coincidence. In the peer-reviewed report of the cohort, almost every person who went on to develop multiple sclerosis had been infected with Epstein-Barr beforehand, and the researchers noted that no known risk factor could explain the pattern.
Why infection alone does not doom anyone
The obvious paradox is that the virus infects roughly nine in ten adults, while multiple sclerosis remains relatively rare. That means Epstein-Barr infection cannot be sufficient on its own to cause the disease; something else must combine with it to tip a small fraction of infected people toward illness. Scientists suspect a mix of genetic susceptibility, immune factors, and possibly other exposures determines who is affected.
One leading hypothesis, explored in reviews such as a Nature Reviews Neuroscience examination of the virus and the disease, is molecular mimicry: some proteins the virus produces resemble proteins in the nervous system closely enough that antibodies made against the virus may cross-react with the body’s own tissue. Other proposed mechanisms involve infected immune cells behaving abnormally. The precise pathway is still being worked out.
What the link could mean for prevention
If Epstein-Barr virus is truly a necessary step toward multiple sclerosis, then blocking the virus could, in principle, prevent many cases. That prospect has intensified interest in developing a vaccine against the virus, and several candidates are in early testing. Researchers are also studying whether antiviral drugs or therapies targeting infected B cells could help people who already have the disease.
None of that is settled, and a vaccine capable of preventing multiple sclerosis remains a hope rather than a reality. But the strength of the evidence has moved Epstein-Barr virus from a background curiosity to a central character in the story of one of the most common disabling neurological diseases of young adults, and given scientists a concrete target to pursue.
It is also a reminder of how long the shadow of a common infection can stretch. A virus caught quietly in childhood, causing little at the time, may help set in motion a disease that surfaces only years or decades later in a small fraction of those exposed. That delayed, probabilistic connection is difficult to see without the kind of enormous, long-running datasets that made the military study possible, and it hints that other chronic diseases may yet be traced to infections once dismissed as harmless.
This article was produced with the assistance of AI and reviewed by Morning Overview editors prior to publication.
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