scholarly journals Epstein-Barr virus infection as a predisposing factor for multiple sclerosis. An update from molecular biology, immunology and epidemiology

2019 ◽  
Vol 67 (3) ◽  
pp. 305-313
Author(s):  
David López-Valencia ◽  
Ángela Medina-Ortega ◽  
Diego Fernando Hoyos-Samboní ◽  
Jhan Sebastián Saavedra-Torres ◽  
Carolina Salguero

Introduction: Epstein-Barr virus is an infectious agent used to immortalize and induce polyclonal activation of B cells. It has been widely described that this virus produces changes in the cells it infects and in the immune response, and stimulates the development of autoimmune diseases.Objective: To characterize the association between Epstein-Barr virus and multiple sclerosis described in current scientific literature.Materials and methods: A 59-years range literature search was conducted in the PubMed, ScienceDirect, Redalyc and SciELO databases using the following MeSH terms: “Epstein-Barr virus, multiple sclerosis autoimmune diseases, autoimmune diseases of the nervous system”.Results: Many studies describe the association between Epstein-Barr virus and multiple sclerosis. It is believed that acute infection and viral reactivation promote the development of multiple sclerosis.Conclusions: It is necessary to conduct further research on the pathogenesis and morphophysiological and neuroimmunological changes –at the ecological, molecular, cellular, tissue, organic and systemic level– induced by the immune response and that favor the development of multiple sclerosis.

Author(s):  
Bert A. ‘t Hart

Abstract Using a non-human primate model of the autoimmune neuroinflammatory disease multiple sclerosis (MS), we have unraveled the role of B cells in the making and breaking of immune tolerance against central nervous system myelin. It is discussed here that B cells prevent the activation of strongly pathogenic T cells present in the naïve repertoire, which are directed against the immunodominant myelin antigen MOG (myelin oligodendrocyte glycoprotein). Prevention occurs via destructive processing of a critical epitope (MOG34-56) through the lysosomal serine protease cathepsin G. This effective tolerance mechanism is abrogated when the B cells are infected with Epstein–Barr virus, a ubiquitous γ1-herpesvirus that entails the strongest non-genetic risk factor for MS.


Brain ◽  
2009 ◽  
Vol 132 (12) ◽  
pp. 3318-3328 ◽  
Author(s):  
Simon N. Willis ◽  
Christine Stadelmann ◽  
Scott J. Rodig ◽  
Tyler Caron ◽  
Stefan Gattenloehner ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document