Highlights
- •Ab response against EBNA1, MAP106c, MBP and HERV-Wenv was evaluated in MS patients.
- •No difference was observed during natalizumab treatment for EBNA1, MAP106c, and MBP.
- •Difference in the Ab response was observed for HERV-Wenv during natalizumab exposure.
- •Natalizumab treatment reduces Ab production against HERV-Wenv in MS patients.
Abstract
Multiple Sclerosis (MS) is a heterogeneous disorder of the central nervous system
(CNS) that begins as an inflammatory autoimmune disorder mediated by auto-reactive
lymphocyte followed by microglial activation and chronic degeneration. The etiology
of Multiple Sclerosis (MS) is unknown but several data support the hypothesis of possible
infectious agents which may act as a trigger for the pathogenic cascade. Human endogenous
retrovirus (HERV-W/MSRV), Epstein Barr Virus (EBV) and Mycobacterium avium ss. paratuberculosis (MAP) have been associated to Multiple Sclerosis. In this study, we evaluated the
humoral response against different peptides: the human endogenous retrovirus HERV-Wenv73–88, MAP106c121–132 from MAP, EBNA1 400–413 from EBV and the homologous human peptide MBP85–98 in a cohort of MS patients treated with natalizumab. Results showed a statistically
significant difference in the response against the HERV-W peptide in MS patients after
two years of natalizumab treatment.
Keywords
To read this article in full you will need to make a payment
Purchase one-time access:
Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online accessOne-time access price info
- For academic or personal research use, select 'Academic and Personal'
- For corporate R&D use, select 'Corporate R&D Professionals'
Subscribe:
Subscribe to Journal of the Neurological SciencesAlready a print subscriber? Claim online access
Already an online subscriber? Sign in
Register: Create an account
Institutional Access: Sign in to ScienceDirect
References
- Infectious causes of multiple sclerosis.Lancet Neurol. 2006; 5: 887-894
- A Sardinian map for multiple sclerosis.Future Microbiol. 2013; 8: 223-232
- Mycobacterium avium ss. paratuberculosis Zoonosis – The Hundred Year War – beyond Crohn's disease.Front. Immunol. 2015; 6: 96
- Are Mycobacterium avium subsp. paratuberculosis and Epstein–Barr virus triggers of multiple sclerosis in Sardinia?.Mult. Scler. 2012; 18: 1181-1184
- Multiple sclerosis-associated retrovirus and progressive disability of multiple sclerosis.Mult. Scler. 2010; 16: 1248-1251
- Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria.Ann. Neurol. 2011; 69: 292-302
- Adhesion molecules are promising candidates to establish surrogate markers for natalizumab treatment.Mult. Scler. 2011; 17: 16-23
- Epstein–Barr virus and Mycobacterium avium subsp. paratuberculosis peptides are cross recognized by anti-myelin basic protein antibodies in multiple sclerosis patients.J. Neuroimmunol. 2014; 270: 51-55
- Natalizumab inhibits the expression of human endogenous retroviruses of the W family in multiple sclerosis patients: a longitudinal cohort study.Mult. Scler. 2014; 20: 174-182
- Natalizumab exerts a suppressive effect on surrogates of B cell function in blood and CSF.Mult. Scler. 2015; 21: 1036-1044
- Natalizumab treatment decreases serum IgM and IgG levels in multiple sclerosis patients.Mult. Scler. 2013; 19: 1454-1461
- Human endogenous retrovirus type W envelope expression in blood and brain cells provides new insights into multiple sclerosis disease.Mult. Scler. 2012; 18: 1721-1736
- Changes to anti-JCV antibody levels in a Swedish national MS cohort.J. Neurol. Neurosurg. Psychiatry. 2013; 84: 1199-1205
Article info
Publication history
Published online: July 08, 2015
Accepted:
July 6,
2015
Received in revised form:
July 3,
2015
Received:
April 10,
2015
Identification
Copyright
© 2015 Elsevier B.V. Published by Elsevier Inc. All rights reserved.
