An Epstein Barr virus-related cross reactive autoimmune response in multiple sclerosis in Norway

Vaughan, John H.; Riise, Trond; Rhodes, Gary; Nguyen, Minh-Duc; Barrett‐Connor, Elizabeth; Nyland, Harald

doi:10.1016/0165-5728(96)00069-0

Cited by 29 publications

(10 citation statements)

References 23 publications

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“…None of the studies were population based. We have previously reported a raised EBV related autoimmune response in patients with multiple sclerosis20 and clustering of places of residence of patients with multiple sclerosis at the ages of 13–20 years,21 which coincides with the ages of high incidence of infectious mononucleosis 9. In the present report, we have studied the seroprevalence of anti-EBV antibodies in the same group of patients with multiple sclerosis and controls from the county of Hordaland.…”

mentioning

confidence: 69%

Altered antibody pattern to Epstein-Barr virus but not to other herpesviruses in multiple sclerosis: a population based case-control study from western Norway

Myhr

Riise

Barrett‐Connor

et al. 1998

Journal of Neurology, Neurosurgery & Psychiatry

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Objective-The prevalence of anti-EBV antibodies was studied in a group of 144 patients with multiple sclerosis and 170 age, sex, and area matched controls from the county of Hordaland, western Norway. The prevalence of three other herpesviruses, herpes simplex virus (HSV), varicella zoster virus (VZV), and cytomegalovirus (CMV), were also included. Methods-Antibodies to various virus antigens were determined by enzyme linked immunosorbent assay (ELISA) and indirect immunfluorescence (IIF) in serum samples from 144 patients with multiple sclerosis and 170 controls. Results-All of the 144 patients with multiple sclerosis had IgG antibodies to EBV compared with 162 of 170 controls (p=0.008). The frequency of IgG antibodies to EBV capsid antigen (VCA), nuclear antigen (EBNA), and early antigen (EA) was significantly higher in patients with multiple sclerosis compared with the controls (p<0.000001, p=0.01, and p<0.0001 respectively). The presence of antibodies was independent of the initial course of the disease and the disease activity at the time of blood sampling. The prevalence of IgG antibodies to HSV, CMV, and VZV did not diVer between cases and controls. Conclusion-The results suggest a role for EBV in the aetiology of multiple sclerosis. (J Neurol Neurosurg Psychiatry 1998;64:539-542)

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confidence: 69%

Altered antibody pattern to Epstein-Barr virus but not to other herpesviruses in multiple sclerosis: a population based case-control study from western Norway

Myhr

Riise

Barrett‐Connor

et al. 1998

Journal of Neurology, Neurosurgery & Psychiatry

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“…Alternatively, EBV could contribute to MS onset acting outside of the central nervous system. One hypothesis is that of molecular mimicry between EBV and myelin antigens, which could involve antibodies (Rand et al 2000;Vaughn et al 1996) or T lymphocytes. (Hollsberg et al 2003;Holmoy et al 2004;Lang et al 2002).…”

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confidence: 99%

Epstein–Barr Virus Infection and Multiple Sclerosis: A Review

Ascherio

Munger

2010

J Neuroimmune Pharmacol

230

186

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Epstein-Barr virus (EBV) infection results in a life-long persistence of the virus in the host's B-lymphocytes and has been associated with numerous cancers including Burkitt's lymphoma, Hodgkin lymphoma, and nasopharyngeal carcinoma. There is considerable evidence that EBV infection is a strong risk factor for the development of multiple sclerosis. Early age at primary EBV infection is typically asymptomatic, but primary infection during adolescence or adulthood often manifests as infectious mononucleosis, which has been associated with a two- to threefold increased risk of MS. Most importantly, MS risk is extremely low in individuals who are EBV negative, but it increases several folds following EBV infection. Additional evidence supporting a role for EBV in MS pathogenesis includes the observations of elevated antibodies to EBV antigens (especially EBV nuclear antigen-1) prior to the onset of MS, and an increased risk of MS among EBV-positive children. The biological mechanism by which EBV may cause MS is not known, but several possibilities are discussed.

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“…Indeed, during viral persistence, housekeeping functions of the cell may not be altered, whereas specialized functions, like the secretion of insulin, may be affected, resulting in pathology at the level of the organism [7 -9]. Other viruses, in particular retro-, corona-and herpesviruses, are proposed to play a role in the development of autoimmune diseases such as multiple sclerosis [10][11][12][13].…”

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confidence: 99%

Molecular mechanisms of poliovirus persistence: key role of capsid determinants during the establishment phase

Pelletier

Duncan

Pavio

et al. 1998

Cellular and Molecular Life Sciences (CMLS)

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As viral persistence is of major medical importance, well-characterized, simple models are needed to improve our understanding of persistent infections. We have chosen to study the molecular mechanisms of viral persistence with the poliovirus (PV), because this picornavirus is one of the best characterized animal viruses, it infects the central nervous system which is a target organ for viral persistence, and it belongs to the Picornaviridae family of viruses, which includes several naturally persisting viruses. We have developed models of PV persistence in neuronal and epidermoid cells, and the present review will focus on the latter one because both lytic and persistent PV strains can be used to study the PV-HEp-2 cell interactions. The viral determinants of persistence have been investigated with this model, and PV determinants have proven to be of crucial importance for the establishment of persistence in HEp-2 cells. Precise determinants of PV persistence have been identified for PV serotypes 1 and 3, in capsid proteins VP1 and VP2. These determinants modify the early steps of the PV cycle, and in particular, the conformational modifications of the capsid following virus adsorption onto its receptor. These results permit us to propose several hypotheses concerning PV persistence and the early steps of the PV cycle.

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An Epstein Barr virus-related cross reactive autoimmune response in multiple sclerosis in Norway

Cited by 29 publications

References 23 publications

Altered antibody pattern to Epstein-Barr virus but not to other herpesviruses in multiple sclerosis: a population based case-control study from western Norway

Altered antibody pattern to Epstein-Barr virus but not to other herpesviruses in multiple sclerosis: a population based case-control study from western Norway

Epstein–Barr Virus Infection and Multiple Sclerosis: A Review

Molecular mechanisms of poliovirus persistence: key role of capsid determinants during the establishment phase

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