NECESSARY but not sufficient. The Epstein-Barr virus really seems to be one of the causes of multiple sclerosis, although not the only one. The factors that can trigger the disease, in fact, are many – both genetic and environmental – and they must be combined together. Among these, the Epstein-Barr virus has long attracted the attention of researchers, whose correlation with the disease is known even if so far, as the same association of patients (AISM) reiterates, it has not been possible to demonstrate with certainty. the cause-effect relationship between its presence and the onset of multiple sclerosis. New evidence of his involvement comes today from a study just published in the pages of Science by the team led by the Italian Alberto Ascherio of the Harvard TH Chan School of Public Health. Evidence so strong that the authors say that what they observed in their study leads to consider Epstein-Barr as one of the causes of multiple sclerosis.
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A very common virus
EBV is a very widespread herpesvirus in the population – it is estimated that it can affect 95% of people – and in most cases it is present without causing symptoms, although it can sometimes manifest itself in the form of mononucleosis (the so-called kissing disease). However, the percentages of infections increase in the population with MS (reaching almost 100%), and some observations – such as the high presence of antibodies against the virus, the appearance of the disease after mononucleosis, and in some cases the presence of the virus in lesions, the authors explain – have led to consider EBV a possible causative agent of MS.
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To understand this, Ascherio’s team therefore reviewed a huge sample of people, some of whom over the years had developed multiple sclerosis, and for whom several blood samples collected over the years were available for analysis. The sample in question is that of over 10 million US soldiers observed over the course of two decades, in which a total of 955 cases of multiple sclerosis have been identified. The analysis then focused on 801 patients and 1566 controls for which comparable samples were available to test for the presence of EBV infection and the evolution of the antibody response to the virus. But the researchers also investigated the presence of a disease marker (a component of neurofilaments, an indicator of damage to axons, the ends of neurons) and the responses of part of the sample to other viral infections (also with similar behavior, such as those from cytomegalovirus) as an additional control.
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Risk increases by 32 times
Putting all the results together, the scientists observed that all but one patients (thus 800) were positive for the virus, and that initially 35 were negative for EBV (107 in controls). Of these 35, 34 then became positive for EBV prior to the onset of multiple sclerosis. For these, the researchers observed a higher conversion rate (from negative to positive for EBV) than the controls. Overall, the risk of developing MS after EBV infection increased 32-fold but did not change after infection with other viruses, the authors write. Levels of the disease marker analyzed also increased only after EBV infection.
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The researchers then critically reviewed the collected data looking for possible confounding factors (both environmental and genetic) or an inverse causal relationship with the virus (i.e. that the disease predisposed to infection and not vice versa), however, finding nothing that could give alternative explanations to what was observed. The conclusion of everything, they write, is that EBV is one of the causes of the onset of multiple sclerosis, and that therefore a vaccine against mononucleosis would also bring benefits in the neurological field, lowering the risk of disease. Helpful, however, and they conclude, could also be antiviral, since the virus also seems to contribute to the pathogenesis of the disease.
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Mechanisms still unknown
We still know little about the mechanisms by which virus infection induces the damage to the nervous system observed in multiple sclerosis, even if different hypotheses are at stake, add William H. Robinson and Lawrence Steinman of Stanford University in a perspective accompanying the item. EBV affects B lymphocytes. Infection of these cells – involved in the disease – could contribute to altering them, or perhaps the mimicry of viral proteins with some components of the nervous system trigger an abnormal autoimmune response, such as that seen in MS patients. . But while recognizing the causal role of EBV infection, given its spread in the general population – almost everyone – it is obvious that other factors must also be present for multiple sclerosis to arise. The virus in substance seems to be a necessary but not sufficient factor, Robinson and Steinman close, for the disease to appear, for which other contributions are needed, such as genetic predisposition.
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