Expression of the Human Herpesvirus 6A Latency-Associated Transcript U94A Disrupts Human Oligodendrocyte Progenitor Migration
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Author
Campbell, Andrew
Hogestyn, Jessica M.
Lopez, Brittany
Pröschel, Christoph
Mock, David
Mayer-Pröschel, Margot
Published Version
https://doi.org/10.1038/s41598-017-04432-yMetadata
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Campbell, Andrew, Jessica M. Hogestyn, Christopher J. Folts, Brittany Lopez, Christoph Pröschel, David Mock, and Margot Mayer-Pröschel. 2017. “Expression of the Human Herpesvirus 6A Latency-Associated Transcript U94A Disrupts Human Oligodendrocyte Progenitor Migration.” Scientific Reports 7 (1): 3978. doi:10.1038/s41598-017-04432-y. http://dx.doi.org/10.1038/s41598-017-04432-y.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.Other Sources
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5479784/pdf/Terms of Use
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http://nrs.harvard.edu/urn-3:HUL.InstRepos:33490764
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