In addition to the link, already ascertained, between multiple sclerosis and the mononucleosis virus, there are genetic factors that predispose to the disease.
In recent years, several studies have confirmed a connection between a virus that 90-95% of the world population meets at least once in life – that of Epstein-Barr, manager of the mononucleosis – and an increased risk of developing multiple sclerosis. Less clear is because such a “democratic” and widespread infection favors the debut of a serious neurodegenerative disease only, and fortunately, in a small portion of individuals. Now a research published in the scientific journal Pnas It helps to shed light on this aspect.
A sensational own goal. There Multiple sclerosis It is an autoimmune disease characterized by an anomalous reaction of the immune defenses, which attack some components of the central nervous system exchanged for foreign agents. In particular to be targeted is the myelinthe coating that isolates and protects the nerve fibers in the brain and spinal cord. An increasingly accredited hypothesis is that, since the Epstein-Barr virus resembles a protein produced by the central nervous system, the antibodies deployed to combat the pathogen “Sbaglino Mira”, ending up attacking the useful molecule.
An intertwining of causes. The new study, conducted by the scientists of the Karolinska Institutet (Sweden) and the Stanford University medical school (United States) confirms this hypothesis and adds an important piece. The risk of developing multiple sclerosis would in fact seem to derive from a combination between the presence of certain antibodies in response to the Epstein Barr virus, together with some genetic characteristics that predispose to the disease.
Attack on myelin. The research group has confirmed that antibodies to a viral protein of the Epstein -Barr virus, called EBNA1, can inadvertently react with a similar protein found in the brain – Glialcam, expressed by the Glia cells, which support neurons and participate in the formation of the myelin sheath. This “exchange of identity” probably contributes to the onset of multiple sclerosis.
Environment + genetics. Scientists sought in the blood of 650 patients with multiple sclerosis and 661 healthy individuals the levels of antibodies directed against the Ebna1 viral protein and self -anti -tear directed against glialcam and two other useful proteins expressed in the brain (ano2 and cryab) and easily exchangeable for viral antigen. High levels of all types of and crazy antibodies have been found in patients with multiple sclerosis.
However, there was a further increase in risk If, in addition to self -anti -tear, there were a specific risk factor for multiple sclerosis, or the absence of a protective genetic variant against this disease.
In short, a certain gene predisposition contributes to the unruly action of antibodies in raising the risk of developing multiple sclerosis.
Signs to be grasped. Now Swedish scientists have the aim of re -establishing the blood samples collected to understand when the antibodies described appear. If these were also present before the onset of the disease, they could be used as biomarkers for an early diagnosis of multiple sclerosisindispensable to intervene more effectively in therapies.
