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Multiple sclerosis: an example of pathogenic viral interaction?

A hypothesis is formulated on viral interaction between HHV-6A and EBV as a pathogenic mechanism in Multiple Sclerosis (MS). Evidence of molecular and genetic mechanisms suggests a link between HHV-6A infection and EBV activation in the brain of MS patients leading to intrathecal B-cell transformati...

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Detalles Bibliográficos
Autor principal: Fierz, Walter
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5330019/
https://www.ncbi.nlm.nih.gov/pubmed/28241767
http://dx.doi.org/10.1186/s12985-017-0719-3
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author Fierz, Walter
author_facet Fierz, Walter
author_sort Fierz, Walter
collection PubMed
description A hypothesis is formulated on viral interaction between HHV-6A and EBV as a pathogenic mechanism in Multiple Sclerosis (MS). Evidence of molecular and genetic mechanisms suggests a link between HHV-6A infection and EBV activation in the brain of MS patients leading to intrathecal B-cell transformation. Consequent T-cell immune response against the EBV-infected cells is postulated as a pathogenic basis for inflammatory lesion formation in the brain of susceptible individuals. A further link between HHV-6A and EBV involves their induction of expression of the human endogenous retrovirus HERV-K18-encoded superantigen. Such virally induced T-cell responses might secondarily also lead to local autoimmune phenomena. Finally, research recommendations are formulated for substantiating the hypothesis on several levels: epidemiologically, genetically, and viral expression in the brain.
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spelling pubmed-53300192017-03-03 Multiple sclerosis: an example of pathogenic viral interaction? Fierz, Walter Virol J Review A hypothesis is formulated on viral interaction between HHV-6A and EBV as a pathogenic mechanism in Multiple Sclerosis (MS). Evidence of molecular and genetic mechanisms suggests a link between HHV-6A infection and EBV activation in the brain of MS patients leading to intrathecal B-cell transformation. Consequent T-cell immune response against the EBV-infected cells is postulated as a pathogenic basis for inflammatory lesion formation in the brain of susceptible individuals. A further link between HHV-6A and EBV involves their induction of expression of the human endogenous retrovirus HERV-K18-encoded superantigen. Such virally induced T-cell responses might secondarily also lead to local autoimmune phenomena. Finally, research recommendations are formulated for substantiating the hypothesis on several levels: epidemiologically, genetically, and viral expression in the brain. BioMed Central 2017-02-28 /pmc/articles/PMC5330019/ /pubmed/28241767 http://dx.doi.org/10.1186/s12985-017-0719-3 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Review
Fierz, Walter
Multiple sclerosis: an example of pathogenic viral interaction?
title Multiple sclerosis: an example of pathogenic viral interaction?
title_full Multiple sclerosis: an example of pathogenic viral interaction?
title_fullStr Multiple sclerosis: an example of pathogenic viral interaction?
title_full_unstemmed Multiple sclerosis: an example of pathogenic viral interaction?
title_short Multiple sclerosis: an example of pathogenic viral interaction?
title_sort multiple sclerosis: an example of pathogenic viral interaction?
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5330019/
https://www.ncbi.nlm.nih.gov/pubmed/28241767
http://dx.doi.org/10.1186/s12985-017-0719-3
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