Evidence is mounting that multiple sclerosis (MS) might be triggered by one of the world’s most ubiquitous viruses. The findings from a recent investigation were featured in the journal Nature Immunology.
The Epstein-Barr virus (EBV) is practically unavoidable and is responsible for what many refer to as “the kissing disease,” also known by its other names, infectious mononucleosis or glandular fever.
Long after initial infection, the virus can persist within the body in a dormant state, even lurking within brain cells. EBV is present in 95 percent of adults and in nearly every individual afflicted with MS—that mysterious autoimmune condition that can strike suddenly, mistakenly directing an attack against sections of the brain’s own nerve fibers.
For decades, scientific speculation has focused on the notion that an EBV reactivation could somehow precipitate the onset of MS. Now, novel research conducted by scientists at the University of California, San Francisco (UCSF) in the United States has uncovered a plausible mechanism.
The researchers observed an elevated presence of “killer cells”—immune cells capable of eliminating viral pathogens—in MS patients. Furthermore, some of these cytotoxic T-cells appear to be specifically programmed to target EBV.
“Investigating these less-understood CD8+ T-cells allows us to connect various pieces of the puzzle and offers us a fresh perspective on how EBV likely contributes to the development of this disorder,” explains neurologist Joe Sabatino of UCSF.
These discoveries bolster the results of a landmark 2022 study involving over 10 million participants, which demonstrated that the risk of developing MS was 32 times higher following EBV infection. No other viral links were identified.
Over the years, scientific inquiry has deepened this established connection. Prior research indicates that the immune system mistakenly identifies cells harboring EBV as “foreign” rather than as part of the body itself.
Consequently, white blood cells termed B-cells start producing antibodies that flag these infected cells for destruction. A surge of T-cell clones is then deployed to execute this directive.
In 2024, a study revealed a sharp increase in T-cells recognizing EBV in the blood of individuals with MS. Approximately 13 percent of these T-cells possessed receptors tailored to detect EBV-infected cells, compared to only 4 percent recognizing influenza antigens.
In the cerebrospinal fluid (CSF), T-cells specific to EBV accounted for 47 percent of all analyzed cells.
The recent UCSF study provides more detailed confirmation of these prior observations.
The investigative team examined blood and CSF samples from 13 MS patients, contrasting them with data from 5 non-MS individuals (including 2 with other forms of neuroinflammation).
In MS patients, the count of EBV-targeting killer T-cells in the CSF, brain, and spinal cord was 100 times greater than their concentration in general circulation.
This striking disparity suggests that the immune system is reacting to a change, potentially an “EBV reawakening” occurring within the central nervous system, leading to an overreaction.
Significantly, markers for EBV were detected in the CSF of most MS patients, with certain viral genes found to be active. One specific gene exhibited activity only in MS patients, and not in EBV carriers who did not have MS.
“The major hope here is that if we can target EBV, we might significantly impact not only MS but other diseases too, improving the lives of a great many people,” states Sabatino.
This extremely common virus presents numerous long-term challenges. EBV reactivation has been linked to lupus, certain cancers, schizophrenia, Long COVID, chronic fatigue syndrome, and dementia.
If researchers can fully elucidate the impact EBV has on the body’s immune response and devise methods to combat it, this knowledge could be instrumental in treating a wide array of ailments, extending well beyond just multiple sclerosis.
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