Ecoclimber
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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.
"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.
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