title: EBV and Autoimmunity.
abstract: Although a role of EBV in autoimmunity is biologically plausible and evidence of altered immune responses to EBV is abundant in several autoimmune diseases, inference on causality requires the determination that disease risk is higher in individuals infected with EBV than in those uninfected and that in the latter it increases following EBV infection. This determination has so far been possible only for multiple sclerosis (MS) and, to some extent, for systemic lupus erythematosus (SLE), whereas evidence is either lacking or not supportive for other autoimmune conditions. In this chapter, we present the main epidemiological findings that justify the conclusion that EBV is a component cause of MS and SLE and possible mechanisms underlying these effects.
authors.affiliation: Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA. aascheri@hsph.harvard.edu.|Harvard Medical School, Boston, MA, USA. aascheri@hsph.harvard.edu.|Department of Epidemiology and Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA. aascheri@hsph.harvard.edu.
authors.forename: Alberto
authors.initials: A
authors.lastname: Ascherio
authors.affiliation: Department of Epidemiology and Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA. kgorham@hsph.harvard.edu.
authors.forename: Kassandra L
authors.initials: KL
authors.lastname: Munger
mesh_terms: D000818:Animals; D015551:Autoimmunity; D020031:Epstein-Barr Virus Infections / Q000276:immunology* / Q000821:virology; D004854:Herpesvirus 4, Human / Q000235:genetics / Q000502:physiology*; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000276:immunology* / Q000821:virology; D009103:Multiple Sclerosis / Q000276:immunology* / Q000821:virology
keywords: Autoimmunity; Epidemiology; Erythematosus; Multiple sclerosis; Risk factors; Systemic lupus