Primary infection with the Epstein-Barr virus and risk of multiple sclerosis

Authors

  • Lynn I. Levin PhD, MPH,

    1. Department of Epidemiology, Division of Preventive Medicine, Walter Reed Army Institute of Research, Silver Spring, MD
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  • Kassandra L. Munger ScD,

    1. Department of Nutrition, Harvard School of Public Health, Boston, MA
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  • Eilis J. O'Reilly ScD,

    1. Department of Nutrition, Harvard School of Public Health, Boston, MA
    2. Department of Epidemiology, Harvard School of Public Health, Boston, MA
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  • Kerstin I. Falk PhD,

    1. Department of Virology, Swedish Institute for Infectious Disease Control, Solna, Sweden
    2. Department of Microbiology, Tumor and Cell Biology, Karolinska Institute, Solna, Sweden
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  • Alberto Ascherio MD, DrPH

    Corresponding author
    1. Department of Nutrition, Harvard School of Public Health, Boston, MA
    2. Department of Epidemiology, Harvard School of Public Health, Boston, MA
    3. Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA
    • Professor of Epidemiology and Nutrition, Harvard School of Public Health, 665 Huntington Ave, Building II, Room 335, Boston, MA 02115
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  • The views expressed are those of the authors and should not be construed to represent the positions of the Department of the Army, Department of the Navy, or Department of Defense.

Abstract

To determine whether multiple sclerosis (MS) risk increases following primary infection with the Epstein-Barr virus (EBV), we conducted a nested case-control study including 305 individuals who developed MS and 610 matched controls selected among the >8 million active-duty military personnel whose serum has been stored in the Department of Defense Serum Repository. Time of EBV infection was determined by measuring antibody titers in serial serum samples collected before MS onset among cases, and on matched dates among controls. Ten (3.3%) cases and 32 (5.2%) controls were initially EBV negative. All of the 10 EBV-negative cases became EBV positive before MS onset; in contrast, only 35.7% (n = 10) of the 28 controls with follow-up samples seroconverted (exact p value = 0.0008). We conclude that MS risk is extremely low among individuals not infected with EBV, but it increases sharply in the same individuals following EBV infection. ANN NEUROL 2010;67:824–830

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