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From the Department of Neurology (Drs. Sundström, Svenningsson, and Forsgren), the Department of Virology (Drs. Juto and Wadell), Umeå University Hospital; the Department of Public Health and Clinical Medicine, Nutritional Research (Dr. Hallmans) and Epidemiology (Dr. Nyström), Umeå University; and the Department of Medical Microbiology (Dr. Dillner), Malmö University Hospital, Lunds University, Sweden.
Address correspondence and reprint requests to Dr. Peter Sundström, Department of Neurology, Norrlands University, Umeå 590185, Sweden; e-mail: peter.sundstrom{at}neuro.umu.se
Objective: To investigate the association between human herpesviruses and multiple sclerosis (MS), as well as between measles virus and MS.
Methods: The authors identified prospectively collected serum samples from 73 MS cases and retrospective sera from 161 MS cases in two population-based serum bank registers. Analyses of IgG antibody responses in cases and matched referents were performed for Epstein-Barr virus (EBV [EBNA-1 and VCA]), human herpesvirus 6 (HHV-6), herpes simplex virus (HSV), varicella zoster virus (VZV), and measles.
Results: All cases showed signs of past EBV infection. High activity to EBNA-1 and HHV-6 significantly (borderline significance for HHV-6) increased the risk for MS in prospective sera. A discrepancy between activities to EBNA-1 and VCA was striking in MS samples collected less than 5 years before relapsing-remitting MS onset, where high activity to EBNA-1 significantly increased, and high VCA activity significantly decreased the risk for MS. There was no support for major causal roles for HSV, VZV, or measles.
Conclusion: Individuals who will develop MS exhibit an altered immune response against the EBV virus characterized by a high IgG activity to EBNA-1 in the absence of high activity to VCA, this being most pronounced in the 5-year period preceding MS onset.
Received October 1, 2003. Accepted in final form February 11, 2004.
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