Multiple Sclerosis (MS) is an autoimmune disease that affects 2.8 million people around the world. The disease causes the immune system to damage the brain and spinal cord, leading to symptoms such as fatigue, vision disturbance, problems with mobility and balance, and cognitive dysfunction. Although the exact cause of MS remains unknown, scientists have suggested a link between MS and the Epstein-Barr virus (EBV) for decades. A new study offers some clues on how this common virus could cause MS in certain people through a phenomenon called molecular mimicry.

The Study

To understand how molecular mimicry works in MS patients, a group of researchers studied blood samples from over 700 people with MS and a similar number without the disease (a control group). The researchers found that antibodies that bind to a protein from EBV, called EBNA1, were increased in MS patients. These antibodies, generated in response to EBNA1, instead of fighting EBV infection, can target a similar-looking protein called alpha-crystallin B (Cryab) found in areas of the brain that become inflamed in MS. Cryab plays a crucial role in protecting against inflammation, and if antibodies are mistakenly targeting this protein, it could explain the symptoms seen in MS.

The study found that Cryab antibodies were present in up to 23% of MS patients and only 7% of controls, suggesting this process could be involved in either the triggering or progression of MS disease in up to one-quarter of patients. However, there is high variation between people with the disease, and there may be several slightly different ways to develop MS. Previous studies have shown that EBNA1 antibodies can also bind to other proteins in the body, such as anoctamin-2 and GlialCAM, which are more common in people with MS. While EBV antibodies are thought to be involved in MS, T cells – soldiers of the immune system that work alongside antibodies – might also be involved.

The researchers also investigated the role of T cells and found that they can likely cross-react to EBNA1 and Cryab in a similar way. Despite these advances in understanding how the immune response to EBV may be involved in MS, researchers still do not fully understand what happens in early disease or what drives progression.

The study sheds light on how the Epstein-Barr virus could cause MS in certain people through molecular mimicry. The study found that Cryab antibodies were present in up to 23% of MS patients and only 7% of controls, suggesting this process could be involved in either the triggering or progression of MS disease in up to one-quarter of patients. However, there is high variation between people with the disease, and there may be several slightly different ways to develop MS. Researchers still do not fully understand what happens in early disease or what drives progression, and more research is needed to understand how T cells fight EBV infection and how these cells may damage the central nervous system. Overall, the findings of this study provide hope for the development of more personalized therapies to ultimately cure MS.

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