June 26, 2014
Study Offers Insight on How Epstein-Barr Virus May Play a Role in MS
An international team has identified clues that may help explain how Epstein-Barr virus, which has been linked to multiple sclerosis, may contribute to the brain inflammation experienced by people who have MS. In active brain lesions (spots of disease activity) in people who had MS in their lifetimes, the researchers found high levels of an inflammation-stimulating chemical (interferon alpha) that helps the body fight viruses, and nearby, immune B cells latently (inactively) infected by Epstein-Barr virus. They did not find signs of active viral infection. The findings may point to a possible mechanism for how the virus might indirectly stimulate MS disease activity.
[Association of innate immune activation with latent Epstein-Barr virus in active MS lesions. J.S. Tzartos, DPhil, G. Khan, PhD, A. Vossenkamper, MD, M. Cruz-Sadaba, PhD, S. Lonardi, MSc, E. Sefia, MSc, A. Meager, PhD, A. Elia, PhD, J.M. Middeldorp, PhD, M. Clemens, PhD, P.J. Farrell, PhD, G. Giovannoni, PhD and U.-C. Meier, Dphil. Published online before print December 7, 2011, doi: 10.1212/WNL.0b013e31823ed057. Neurology January 3, 2012 vol. 78 no. 1 15-23]
Dr. U.-C. Meier (Queen Mary University of London, UK) and colleagues examined brain specimens from seven people who had had MS, and eleven people who had had other disorders or neurological diseases. They found suggestions of latent Epstein-Barr virus infection in all samples of active MS lesions from the specimens, and also in cases of stroke and central nervous system lymphoma (both of which are conditions involving inflammation), but not in other specimens. The authors outlined additional research needed to confirm and expand these findings and their implications.
An accompanying editorial by Epstein-Barr virus expert Dr. Jan D. Lünemann (University of Zurich) notes that although there have been conflicting studies as to the involvement of this virus in MS, this study is intriguing because it suggests a mechanism by which a latent virus, rather than active viral infection, might indirectly stimulate or maintain central nervous system inflammation in MS.