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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Nature Portfolio
2017
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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) |
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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 |
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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 |
work_keys_str_mv |
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1718394423002267648 |