Research Article| Volume 357, ISSUE 1-2, P106-108, October 15, 2015

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Natalizumab modulates the humoral response against HERV-Wenv73–88 in a follow-up study of Multiple Sclerosis patients


      • 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.


      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.


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