Multiple sclerosis, or MS, is a long-term disease that affects the brain and spinal cord.
Around 2.8 million people worldwide live with the condition, which can cause problems with movement, vision, balance, sensation and thinking.
In MS, the immune system mistakenly attacks myelin, the protective covering around nerve fibers. When this covering becomes damaged, messages between the brain and the rest of the body can slow down or become disrupted.
Scientists have spent decades trying to understand what starts this immune attack. Genetics can influence a person’s risk, and factors such as smoking and low vitamin D have also been linked to MS, but none of these fully explains why the disease develops.
One of the strongest clues involves Epstein-Barr virus, or EBV. This extremely common virus infects about 95% of adults and is best known for causing infectious mononucleosis, sometimes called mono or glandular fever.
After someone becomes infected, EBV usually remains quietly inside the body for life. Because the virus is so common while MS is relatively rare, proving that EBV plays a major role in the disease has been difficult.
A large study led by Professor Alberto Ascherio and researchers at Harvard provided some of the strongest evidence so far that EBV infection is a major trigger for MS. The research was published in the journal Science.
The team studied health information from more than 10 million young adults who served in the U.S. military. Service members regularly provided blood samples, giving researchers an unusual opportunity to see when people became infected with EBV and what happened years later.
Among this enormous group, 955 people were eventually diagnosed with MS during their military service. The researchers examined stored blood samples taken before and after EBV infection and compared the results with people who did not develop MS.
The pattern was striking. The risk of developing MS increased about 32-fold after infection with EBV, while infection with other viruses did not show the same connection.
The researchers also measured neurofilament light chain, a substance released into the blood when nerve cells are damaged. Levels began to rise only after EBV infection, suggesting that signs of injury to the nervous system appeared after people caught the virus.
These results helped researchers address an important question: could people who were already developing MS simply be more likely to catch EBV? The timing seen in the blood samples instead showed that EBV infection came before detectable signs of nerve damage and before an MS diagnosis.
MS often does not appear immediately after EBV infection. Years can pass before clear symptoms develop, possibly because damage builds slowly or because the virus sets off a complicated immune process that takes time to affect the nervous system.
The findings do not mean that everyone infected with EBV will develop MS. Almost all adults eventually carry the virus, while only a small percentage develop MS, showing that other genetic, immune and environmental factors must also influence who becomes ill.
Still, the research suggests that preventing EBV infection could potentially prevent many cases of MS. That possibility has increased scientific interest in vaccines designed to protect people from EBV before they become infected.
Researchers are also interested in antiviral medicines and other treatments that could target EBV or the immune response it triggers. Whether such approaches can prevent MS or improve the disease after it has developed will require further clinical studies.
The discovery gives scientists a clearer direction in a disease whose origins have long been difficult to explain. If researchers can learn exactly how EBV helps trigger MS, they may eventually find new ways to prevent the disease rather than only treating its effects after they appear.
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