Epstein–Barr virus nuclear antigen-1 B-cell epitopes in multiple sclerosis twins

Mechelli, Rosella; Anderson, Jourdan; Vittori, Daniela; Coarelli, Giulia; Annibali, Viviana; Cannoni, Stefania; Aloisi, Francesca; Salvetti, Marco; Ja, James; Ristori, Giovanni

doi:10.1177/1352458511410515

Cited by 25 publications

(23 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Among the observations that remained unexplained are the change in risk among migrants (Gale and Martyn 1995), a probable MS outbreak in the Faroe islands (Kurtzke and Heltberg 2001), and the increasing MS frequency among African-Americans in the USA (Wallin et al 2012) and among women in several countries in North America (Orton et al 2006) and Europe (Koch-Henriksen and Sorensen 2010). One possibility is that there are genetic variations in EBV itself that modulate its propensity to cause MS. A few reports have addressed this hypothesis (Munch et al 1998;Lindsey et al 2008;Mechelli et al 2011) as well as interactions with genetic or environmental factors, which could include other infectious agents.…”

Section: Summary On Ebv and Msmentioning

confidence: 98%

EBV and Autoimmunity

Ascherio

Munger

2015

Current Topics in Microbiology and Immunology

101

View full text Add to dashboard Cite

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.

show abstract

Section: Summary On Ebv and Msmentioning

confidence: 98%

EBV and Autoimmunity

Ascherio

Munger

2015

Current Topics in Microbiology and Immunology

101

View full text Add to dashboard Cite

show abstract

“…In MS, the strongest disease association has been demonstrated to a C-terminal EBNA-1 domain comprising amino acids (aa) 385–420 [40,41]. In a recent study including nine MS-discordant monozygotic twins, this was further narrowed down to aa 401–411, revealing increased response against this epitope in affected compared to healthy co-twins [42]. Lünemann and colleagues have demonstrated that children with MS have a broader IgG response against all three domains of the EBNA-1 protein and that some of the responses against the glycine-alanine repeat domain (aa 88–323) are directed against epitopes not found in the sera of demographically matched healthy peers [43].…”

Section: Evidence Of Associationmentioning

confidence: 99%

Epstein-Barr Virus in Systemic Lupus Erythematosus, Rheumatoid Arthritis and Multiple Sclerosis—Association and Causation

Lossius

Johansen

Torkildsen

et al. 2012

Viruses

113

View full text Add to dashboard Cite

Epidemiological data suggest that the Epstein-Barr virus (EBV) is associated with several autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis and multiple sclerosis. However, it is not clear whether EBV plays a role in the pathogenesis of these diseases, and if so, by which mechanisms the virus may contribute. In this review, we discuss possible viral and immunological mechanisms that might explain associations between EBV and autoimmune diseases and whether these associations represent causes or effects of inflammation and autoimmunity.

show abstract

“…The GA-rich region has been described as the primary target of the normal peripheral humoral immune response (92)(93)(94)(95)97). This is verified by our data.…”

Section: Cryab: Igg Binding the N-terminal Region Maymentioning

confidence: 99%

High-Density Peptide Microarray Analysis of IgG Autoantibody Reactivities in Serum and Cerebrospinal Fluid of Multiple Sclerosis Patients

Hecker

Fitzner

Wendt

et al. 2016

Molecular & Cellular Proteomics

View full text Add to dashboard Cite

Intrathecal immunoglobulin G (IgG Multiple sclerosis (MS)1 is a chronic disease of the central nervous system (CNS) that typically affects young adults, especially women. The disease is characterized by discrete areas of inflammation (lesions), demyelination, axonal loss, and astrogliosis in the brain and spinal cord. The clinical correlate of these processes is a wide range of neurological signs and symptoms involving mobility problems, vision problems, cognitive dysfunction, fatigue, and pain (1, 2). This

show abstract

Epstein–Barr virus nuclear antigen-1 B-cell epitopes in multiple sclerosis twins

Abstract: In a study that controls for confounders, our data focus an EBNA-1 specificity that may be associated with MS pathogenesis.

Cited by 25 publications

References 24 publications

EBV and Autoimmunity

EBV and Autoimmunity

Epstein-Barr Virus in Systemic Lupus Erythematosus, Rheumatoid Arthritis and Multiple Sclerosis—Association and Causation

High-Density Peptide Microarray Analysis of IgG Autoantibody Reactivities in Serum and Cerebrospinal Fluid of Multiple Sclerosis Patients

Contact Info

Product

Resources

About