Format

Send to

Choose Destination
See comment in PubMed Commons below
Immunopharmacol Immunotoxicol. 2012 Feb;34(1):21-35. doi: 10.3109/08923973.2011.572262. Epub 2011 Apr 12.

Epstein-Barr and other viral mimicry of autoantigens, myelin and vitamin D-related proteins and of EIF2B, the cause of vanishing white matter disease: massive mimicry of multiple sclerosis relevant proteins by the Synechococcus phage.

Author information

1
PolygenicPathways, Saint Leonards-on-sea, East Sussex, UK. Chris_car@yahoo.com

Abstract

The Epstein-Barr virus expresses proteins containing numerous short consensi (identical pentapeptides at least, or longer gapped consensi) that are identical to those in 16 multiple sclerosis autoantigens or in the products of multiple sclerosis susceptibility genes. Other viruses implicated in multiple sclerosis also display such mimicry and the Synechococcus phage was identified as a novel and major contributor to this phenomenon. Cyanobacteria hosts of Synechococcus phage favor temperate climes, in line with multiple sclerosis distribution, and bacterial and phage ecology accords closely with multiple sclerosis epidemiology. Bovine, ovine or canine viral proteins were also identified as autoantigen homologues, in line with epidemiological data linking multiple sclerosis to cattle density, sheep contact and dog ownership. Viral proteins align with known autoantigens, other myelin and vitamin D-related proteins and the translation initiation factor EIF2B, which is implicated in vanishing white matter disease. These data suggest that the autoantigens in multiple sclerosis, which causes demyelination in animal models, may be generated by antibodies raised to viral protein homologues. Multiple autoantibodies may cause multiple sclerosis via protein knockdown and immune activation. Their selective removal may be of clinical benefit as already suggested by promising results using plasmapheresis or immunoadsorption in certain multiple sclerosis patients.

PMID:
21486137
DOI:
10.3109/08923973.2011.572262
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Taylor & Francis
    Loading ...
    Support Center