Scientists have taken a significant step toward explaining why the Epstein-Barr Virus (EBV) triggers Multiple Sclerosis (MS) in some individuals, while the vast majority of the population carries the virus without health issues.
The study reveals that the primary cause lies in a genetic factor, specifically the HLA-DR15 molecule. This molecule acts as a “sentinel” for the immune system, appearing on the cell surface to signal what is happening inside the cell.
When B-cells infected with EBV possess the HLA-DR15 genetic package, the virus alters their genetic programming in a way that causes myelin proteins to appear on the cell surface. This process is biologically unusual, as myelin is strictly the insulating sheath of nerve fibers and typically has nothing to do with immune cells. Due to this “disguise,” the immune system is misled; it perceives myelin as a threat and launches an attack against its own nervous tissue.
This autoimmune destruction of the protective nerve fiber coating is precisely what causes Multiple Sclerosis, eventually manifesting as vision impairment, loss of muscle control, and sensory problems.
It is noteworthy that genetics and the virus alone are not enough to trigger the disease. The timing of infection also influences the development of MS—the adolescent period is particularly high-risk. Additionally, contributing factors include:
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Vitamin D deficiency
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Smoking
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Obesity
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Environmental pollution
However, HLA-DR15 remains the most significant genetic risk factor, as every second patient with Multiple Sclerosis carries this specific genetic trait.
Scientists believe that deciphering this mechanism will be a fundamental breakthrough in developing therapeutic strategies and vaccines. While the near-universal prevalence of EBV makes prevention nearly impossible, early-age immunization could play a decisive role. By preventing acute forms of the disease—specifically infectious mononucleosis—the risk of developing MS in the future could be proportionally reduced.
