A common childhood virus is now tied to multiple sclerosis years later

Multiple sclerosis has long been one of neurology’s harder puzzles, a disease in which the immune system attacks the nervous system for reasons that were never fully clear. In January 2022, a large study in the journal Science added the strongest evidence yet that a single, extraordinarily common virus is a driving cause. The virus is Epstein-Barr, a herpesvirus that most people catch, often without knowing it, and the disease it has been connected to can surface years or even decades after that first infection.

The connection is notable precisely because almost everyone carries the virus while only a small fraction ever develop multiple sclerosis. That gap means Epstein-Barr infection is best understood as a likely necessary trigger rather than a guarantee of illness, a distinction that shapes how scientists interpret the finding and what it could eventually mean for prevention.

Epstein-Barr virus infects most people, usually early in life

Epstein-Barr is among the most widespread human viruses. According to the Centers for Disease Control and Prevention, it is the main cause of infectious mononucleosis and spreads mainly through saliva, with the great majority of adults infected at some point. Many pick it up in childhood, when the infection often causes no symptoms or nothing more than a passing mild illness.

When infection is delayed until adolescence or early adulthood, it is more likely to produce the fever, sore throat and swollen lymph nodes of mononucleosis. Either way, the virus is never fully cleared. It settles into a lifelong latent state in certain immune cells, quietly persisting long after the initial illness has faded, which is part of what makes its downstream effects so difficult to trace.

A 2022 analysis of military recruits found a 32-fold jump

The pivotal study drew on stored blood samples from more than 10 million young adults on active duty in the United States military, a group tested repeatedly over years of service. Researchers identified hundreds of people who developed multiple sclerosis and looked back at whether they had been infected with Epstein-Barr before their diagnosis. The risk of developing multiple sclerosis rose roughly 32-fold after infection with the virus.

Crucially, no comparable spike followed infection with other viruses, including cytomegalovirus, which spreads in similar ways. The team also found that a marker of nerve damage in the blood began rising only after Epstein-Barr infection, not before, strengthening the case that the virus preceded and helped set off the disease process rather than merely accompanying it.

Multiple sclerosis is the immune system attacking myelin

To understand why a common virus could matter, it helps to know what goes wrong in the disease. The National Institute of Neurological Disorders and Stroke describes multiple sclerosis as a condition in which the immune system mistakenly attacks myelin, the protective sheath around nerve fibers in the brain and spinal cord. The resulting scar-like lesions disrupt the signals traveling along those nerves.

That damage can produce vision problems, muscle weakness, numbness, fatigue and difficulties with balance and coordination, often coming and going in unpredictable waves. Because the disease reflects an immune system turned against the body’s own tissue, an infection that reshapes immune behavior is a plausible instigator, and Epstein-Barr is known to take up long-term residence in the very immune cells involved.

Near-universal infection but a rare disease

The obvious tension in the findings is that Epstein-Barr is nearly universal while multiple sclerosis is uncommon. If the virus were sufficient on its own, the disease would be far more prevalent than it is. Researchers therefore describe the infection as one component among several, most likely acting together with genetic susceptibility and other environmental factors that determine which infected people go on to develop the illness.

That framing keeps the finding from overreaching. The evidence points to Epstein-Barr as a leading cause and probably a required step for most cases, but it does not prove the virus is the sole cause in every patient, nor does it identify exactly why a particular individual crosses from harmless lifelong infection into autoimmune disease.

What a causal link could mean for prevention

If Epstein-Barr is indeed an essential trigger, then blocking or clearing it becomes a target for heading off multiple sclerosis before it starts. That prospect has intensified interest in an Epstein-Barr vaccine, which could in principle prevent the infection, and in antiviral strategies aimed at the virus in people already carrying it. Both remain under investigation rather than established treatments.

The practical caveats are considerable. Because infection is so common and the disease so rare, any preventive approach would have to be extremely safe to justify wide use, and years of research would be needed to show that reducing infection actually lowers disease rates. The 2022 evidence reframed multiple sclerosis as potentially preventable in a way it had not been before, while leaving the hardest work, turning that insight into a therapy, still ahead.

This article was produced with the assistance of AI and reviewed by Morning Overview editors prior to publication.

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