The 12th Invest in ME Conference, Part 1
OverTheHills presents the first article in a series of three about the recent 12th Invest In ME international Conference (IIMEC12) in London.
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Could EBV be involved in NMO as well?

Discussion in 'Other Health News and Research' started by Ecoclimber, Dec 4, 2014.

  1. Ecoclimber

    Ecoclimber Senior Member

    Permission to Repost by Prof. G

    "This is the first time I have become aware of a potential link between NMO and EBV. Could EBV be a non-specific trigger of CNS inflammatory diseases?

    The study shows than people with NMO, or NMOers, are more likely to antibodies to a protein of EBV called early antigen or EA. This protein is produced as part of early lytic EBV infection and indicates recent viral activation.

    Could this be a clue that NMO onset, and NMO attacks, are triggered non-specifically by infections?

    This is not dissimilar to what occurs in MS; i.e. in about a third of relapses we can identify an infectious trigger in the so called at risk period which is defined as broadly as being 5-6 weeks before the relapse and 1 week after the relapse.

    This has implications for considering the pathogenesis or cause of NMO and MS."


    Epub: Masuda et al. Epstein-Barr virus persistence and reactivation in neuromyelitis optica. J Neurol Neurosurg Psychiatry. 2014 Nov 28. pii: jnnp-2014-308095. doi: 10.1136/jnnp-2014-308095.

    BACKGROUND: Epstein-Barr virus (EBV) infection has been thought to be a key environmental factor in the development of multiple sclerosis (MS). The aim of this study is to investigate the association of EBV infection with neuromyelitis optica (NMO).

    METHODS: We measured levels of serum antibodies against EBV antigens, including anti-viral capsid antigen (VCA) IgM, anti-VCA IgG, anti-early antigen (EA) IgM, anti-EA IgG and anti-EBV nuclear antigen-1 IgG, in 50 NMOers (including 12 partial form with antiaquaporin 4 antibodies), 51 MSers, and 52 healthy controls, and cerebrospinal fluid (CSF) antibodies in 37 NMOers and 33 MSers with ELISA.

    RESULT: Compared with MSers and normal participants, NMOers more frequently had serum anti-EA IgG antibodies (52%), indicating more active viral replication than patients with MS (26%) and controls (25%). The antibody titres were significantly higher in the NMO group than in the MS (p=0.005) and control (p=0.005) groups. The CSF antibody titres were also higher in patients with NMO than in those with MS (p=0.03).

    CONCLUSIONS: Our results raise the hypothesis that persistent, active EBV replication is present in NMO, and may contribute to the immunological alterations that play a pathogenetic role in the disorder.
    Last edited: Dec 4, 2014

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