[Multiple sclerosis and the Epstein-Barr Virus: Current perspectives on their pathogenic mechanisms].

Abstract

The Epstein-Barr virus (EBV) is a herpesvirus that infects more than 90% of the world's population and is implicated in various diseases, including lymphoproliferative and neoplastic disorders. Recently, evidence has suggested a strong association between EBV and multiple sclerosis (MS). Although EBV infection is common, only a minority of carriers develop MS, indicating the influence of genetic and environmental factors in the pathogenesis. This article reviews the molecular mechanisms through which EBV might influence the development of MS. One mechanism discussed is molecular mimicry, where the similarity between EBV viral antigens and central nervous system proteins could induce a cross-reactive autoimmune response. Additionally, the mechanisms by which EBV evades the immune response are reviewed, including the expression of proteins such as EBNA1 and EBNA2, which interfere with the function of T and NK cells. Genetic factors, such as the HLA-DRB1*15:01 allele, a principal risk factor for MS, are also reviewed. This allele acts as a co-receptor facilitating the infection of B cells by EBV, which could explain the increased susceptibility to MS in individuals with this allele. Furthermore, EBV may alter the epigenetic regulation of genes associated with MS, affecting the expression of key genes in immune response and inflammation. Finally, immunotherapies targeting EBV, such as those based on cytotoxic T lymphocytes, are discussed.