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.

Increased risk of rheumatoid arthritis among mothers with children who carryDRB1risk-associated alleles

“…DRB1*04:01 does not have a strong association with SLE but it does share sequence similarities with the Epstein–Barr virus (EBV)35; EBV is a risk factor for SLE 36. Studies in RA have demonstrated that ACPAs react with EBV viral sequences and may contribute to disease-associated antibody formation 37.…”

The common marmoset (<i>Callithrix jacchus</i>): a relevant preclinical model of human (auto)immune-mediated inflammatory disease of the brain

“…There is strong evidence for a pathogenic role of EBV infection, but the discrepancy between the high prevalence of EBV infection in the human population (> 90 %) and the low incidence of MS (±0.1 %) is unexplained (Ascherio et al, 2012). The risk for MS increases 2-3-fold with development of infectious mononucleosis compared to EBVseropositive people, and an increased IgG1 titer against EBV proteins EBNA-1 is predictive of disease exacerbation (Ascherio and Munger, 2015). MS development is virtually not seen in EBV-seronegative individuals (Pakppor et al, 2013), providing further evidence of a link between EBV and MS. Critical to this discussion, and as previously mentioned, is the fact that marmosets are naturally infected with an EBV homolog (CalHV3).…”

Elimination of Nucleoproteins in Systemic Lupus Erythematosus and Antinuclear Autoantibodies Production

“…Although this "trigger agent" is not deinitely identiied, a wide spectrum of viruses, including Epstein-Barr virus, retroviruses, and herpesviruses, could make a substantial contribution [10]. Other inluencing factors are insolation, drugs, and some pollutants.…”