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Sci Rep. 2017 Jun 21;7(1):3978. doi: 10.1038/s41598-017-04432-y.

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

Author information

1
Department of Biomedical Genetics, University of Rochester, School of Medicine and Dentistry, 601 Elmwood Avenue, Box 633, NY, 14642, USA.
2
Environmental Health Science Center, University of Rochester, School of Medicine and Dentistry, 601 Elmwood Avenue, Box 633, Rochester, NY, 14642, USA.
3
Department of Neuroscience, School of Medicine and Dentistry, University of Rochester, 601 Elmwood Avenue, Box 633, Rochester, NY, 14642, USA.
4
Division of Newborn Medicine, Boston Children's Hospital/Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA.
5
Department of Biomedical Genetics, University of Rochester, School of Medicine and Dentistry, 601 Elmwood Avenue, Box 633, NY, 14642, USA. David_mock@urmc.rochester.edu.
6
Department of Biomedical Genetics, University of Rochester, School of Medicine and Dentistry, 601 Elmwood Avenue, Box 633, NY, 14642, USA. Margot_mayer-proschel@urmc.rochester.edu.
7
Environmental Health Science Center, University of Rochester, School of Medicine and Dentistry, 601 Elmwood Avenue, Box 633, Rochester, NY, 14642, USA. Margot_mayer-proschel@urmc.rochester.edu.
8
Department of Neuroscience, School of Medicine and Dentistry, University of Rochester, 601 Elmwood Avenue, Box 633, Rochester, NY, 14642, USA. Margot_mayer-proschel@urmc.rochester.edu.

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.

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