Expression of the Human Herpesvirus 6A Latency-Associated Transcript U94A Disrupts Human Oligodendrocyte Progenitor Migration

Abstract Progression of demyelinating diseases is caused by an imbalance of two opposing processes: persistent destruction of myelin and myelin repair by differentiating oligodendrocyte progenitor cells (OPCs). Repair that cannot keep pace with destruction results in progressive loss of myelin. Vira...

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Autores principales: Andrew Campbell, Jessica M. Hogestyn, Christopher J. Folts, Brittany Lopez, Christoph Pröschel, David Mock, Margot Mayer-Pröschel
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Publicado: Nature Portfolio 2017
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Acceso en línea:https://doaj.org/article/c31090ca82e3444daa7a868ec7878e14
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spelling oai:doaj.org-article:c31090ca82e3444daa7a868ec7878e142021-12-02T12:30:19ZExpression of the Human Herpesvirus 6A Latency-Associated Transcript U94A Disrupts Human Oligodendrocyte Progenitor Migration10.1038/s41598-017-04432-y2045-2322https://doaj.org/article/c31090ca82e3444daa7a868ec7878e142017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-04432-yhttps://doaj.org/toc/2045-2322Abstract Progression of demyelinating diseases is caused by an imbalance of two opposing processes: persistent destruction of myelin and myelin repair by differentiating oligodendrocyte progenitor cells (OPCs). Repair that cannot keep pace with destruction results in progressive loss of myelin. Viral infections have long been suspected to be involved in these processes but their specific role remains elusive. Here we describe a novel mechanism by which HHV-6A, a member of the human herpesvirus family, may contribute to inadequate myelin repair after injury.Andrew CampbellJessica M. HogestynChristopher J. FoltsBrittany LopezChristoph PröschelDavid MockMargot Mayer-PröschelNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-7 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Andrew Campbell
Jessica M. Hogestyn
Christopher J. Folts
Brittany Lopez
Christoph Pröschel
David Mock
Margot Mayer-Pröschel
Expression of the Human Herpesvirus 6A Latency-Associated Transcript U94A Disrupts Human Oligodendrocyte Progenitor Migration
description Abstract Progression of demyelinating diseases is caused by an imbalance of two opposing processes: persistent destruction of myelin and myelin repair by differentiating oligodendrocyte progenitor cells (OPCs). Repair that cannot keep pace with destruction results in progressive loss of myelin. Viral infections have long been suspected to be involved in these processes but their specific role remains elusive. Here we describe a novel mechanism by which HHV-6A, a member of the human herpesvirus family, may contribute to inadequate myelin repair after injury.
format article
author Andrew Campbell
Jessica M. Hogestyn
Christopher J. Folts
Brittany Lopez
Christoph Pröschel
David Mock
Margot Mayer-Pröschel
author_facet Andrew Campbell
Jessica M. Hogestyn
Christopher J. Folts
Brittany Lopez
Christoph Pröschel
David Mock
Margot Mayer-Pröschel
author_sort Andrew Campbell
title Expression of the Human Herpesvirus 6A Latency-Associated Transcript U94A Disrupts Human Oligodendrocyte Progenitor Migration
title_short Expression of the Human Herpesvirus 6A Latency-Associated Transcript U94A Disrupts Human Oligodendrocyte Progenitor Migration
title_full Expression of the Human Herpesvirus 6A Latency-Associated Transcript U94A Disrupts Human Oligodendrocyte Progenitor Migration
title_fullStr Expression of the Human Herpesvirus 6A Latency-Associated Transcript U94A Disrupts Human Oligodendrocyte Progenitor Migration
title_full_unstemmed Expression of the Human Herpesvirus 6A Latency-Associated Transcript U94A Disrupts Human Oligodendrocyte Progenitor Migration
title_sort expression of the human herpesvirus 6a latency-associated transcript u94a disrupts human oligodendrocyte progenitor migration
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/c31090ca82e3444daa7a868ec7878e14
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