Scientists Discover New Evidence a Common Virus Helps Trigger MS
NEWS | 04 March 2026
Evidence is mounting that multiple sclerosis (MS) may be triggered by one of the most common viruses in the world. The Epstein-Barr virus (EBV) is virtually unavoidable, responsible for what many people refer to as 'kissing disease', otherwise known as infectious mononucleosis or glandular fever. Long after exposure, the virus can lie dormant in the body, hiding even in brain cells. EBV is carried by 95 percent of adults and virtually everyone with MS – a mysterious autoimmune disease that can come on suddenly and mistakenly attack parts of the brain's own nerve fibers. For decades now, scientists have hypothesized that a flare-up of EBV may somehow be triggering the onset of MS. Now, a new study, led by researchers at the University of California San Francisco (UCSF) in the US, has found a plausible mechanism. The team has discovered that 'killer' T cells, immune players that can destroy viral pathogens, are more abundant in MS patients. What's more, some of these killer T cells appear to be specifically tuned to EBV. "Looking at these understudied CD8+ T cells connects a lot of different dots and gives us a new window on how EBV is likely contributing to this disease," says neurologist Joe Sabatino at UCSF. The findings follow a groundbreaking study in 2022 of more than 10 million people, which found that the risk of MS is 32 times higher after an EBV infection. No other viral connections were found. In the years since, research has dug further into the connection. Past research suggests that the immune system recognizes cells that harbor EBV as 'foreigners' rather than part of the body. As a result, white blood cells called B cells produce antibodies that tag these cells for destruction. Then, along comes an army of T cell clones to do their bidding. In 2024, a study found that in the blood of patients with MS, T cells that recognized EBV had exploded in number. Roughly 13 percent of T cells had receptors recognizing EBV-infected cells, and yet only 4 percent recognized antigens for the flu. In the cerebrospinal fluid (CSF), T cells that recognized EBV represented 47 percent of the analyzed cells. The new research from UCSF supports those findings with a little more detail. The team analyzed the blood and CSF of 13 patients with MS, compared to 5 people without MS (including 2 with other neuro-inflammatory disorders). In MS patients, killer T cells that recognized EBV proteins were up to 100 times more abundant in the CSF, around the brain and spinal cord, than in wider blood circulation. This is a large difference that suggests the immune system is responding to a change, possibly a 'reawakening' of the EBV virus in the central nervous system, leading to an overreactive response. Importantly, most MS patients had markers of EBV present in their CSF, and some of the virus's genes were active. One of these genes was active only in patients with MS, not in those without MS who also harbored EBV. Related: First-Ever Vaccine Candidate Against Epstein-Barr Delivers Promising Results "The big hope here is that if we can interfere with EBV, we can have a big effect, not just on MS but on other disorders, and improve the quality of life for many, many people," says Sabatino. This super-common virus is proving quite meddlesome in the long run. A flare-up of EBV is linked to lupus, certain cancers, schizophrenia, long COVID, chronic fatigue syndrome, and dementia. If researchers can figure out what EBV is doing to the body's immune system, and what to do about it, it could help us treat numerous illnesses and diseases, not just MS. The study was published in Nature Immunology.
Author: Carly Cassella.
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