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人类疱疹病毒 6A 潜伏相关转录物 U94A 的表达破坏人类少突胶质前体细胞的迁移。

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

机构信息

Department of Biomedical Genetics, University of Rochester, School of Medicine and Dentistry, 601 Elmwood Avenue, Box 633, NY, 14642, USA.

Environmental Health Science Center, University of Rochester, School of Medicine and Dentistry, 601 Elmwood Avenue, Box 633, Rochester, NY, 14642, USA.

出版信息

Sci Rep. 2017 Jun 21;7(1):3978. doi: 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.

摘要

脱髓鞘疾病的进展是由两个相反过程的失衡引起的

髓磷脂的持续破坏和分化的少突胶质前体细胞(OPC)的髓磷脂修复。修复不能与破坏同步进行,导致髓磷脂逐渐丧失。病毒感染长期以来一直被怀疑与这些过程有关,但它们的具体作用仍不清楚。在这里,我们描述了人类疱疹病毒家族的一员 HHV-6A 可能有助于损伤后髓磷脂修复不足的新机制。

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