A fortnight ago, the journal Science published the results of a recent study that directly relates the development of multiple sclerosis to the Epstein-Barr virus (EBV). The link between the EBV infection and multiple sclerosis has long been discussed in previous studies as well as clinical practice. However, research shared in Science indicates a 32 times higher risk of developing multiple sclerosis in those infected with EBV; the same does not apply to other pathogens of the same family such as the cytomegalovirus (CMV).
Shortly after, on January 24th, the results of another study led by Stanford Medicine appeared in Nature: “Clonally Expanded B Cells in Multiple Sclerosis Bind EBV EBNA1 and GlialCAM“, identifying how Epstein-Barr virus triggers multiple sclerosis, namely by mimicking a protein made in the brain and spinal cord, which leads immunity to mistakenly attack the body’s nerve cells. Evidence on EBV’s implication in MS is thus compelling, whereby the virus has become the most important therapeutic target for MS prevention and treatment. “If a virus is the target of the immune response that’s going an unwanted way in the MS brain, why not get rid of the virus?”, said William Robinson, senior author of the paper (read the news on Stanford Medicine’s webpage).
Two years ago, Dr Walter Wührer, MD, published an article on our behalf entitled “The Epstein-Barr virus: possible role in the development of multiple sclerosis“, wherein multiple sclerosis is defined as a multifactorial disease. An inflammatory environment is listed among the risk factors, which also include infections, EBV being “considered one of the most significant triggers of infectious origin for this autoimmune disease”. The article also brings together the evidence on the role of EBV in multiple sclerosis and the potential mechanisms of virus-associated autoimmunity. In this respect, and given the implication of EBV in the pathogenesis of MS, Dr Wührer’s article suggests that micro-immunotherapy may contribute to preventing the onset of virus-associated autoimmunity by supporting the antiviral defence and hindering the reactivation of viruses such as EBV.
The findings published in Science and Nature confirm the importance of supporting immunity against latent viruses that can reactivate, like herpesviruses. It should be borne in mind that over 90% of the world population is infected with EBV. Although the virus has been associated with autoimmune and oncogenic processes, its effects on the body largely depend on the status of the immune system and its ability to keep the virus under control.
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