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根治唇疱疹新法

    美国研究人员在英国《自然》(Nature)杂志上撰文说,因单纯疱疹病毒引起的唇疱疹也许会成为过去式.
    研究人员说,他们已发现一种隐蔽机制,它能让病毒在被激活之前躲藏在面部神经中.激活办法包括暴晒或发烧等.
    这种病毒名为HSV1,是其首字母缩写.在病毒被激活以前,它能藏匿多年,任何药物都无效.当它苏醒后,会立即在唇部之前发病的同一部位引发炎症.
    由杜克大学医学中心的分子基因学和微生物学教授布莱恩•卡伦带领的小组,深入研究了HSV1是如何能在这些潜伏阶段和活跃阶段之间切换的.他们发现,答案就在病毒休眠时产生的唯一物质之中.其产物是名为LAT核糖核酸(RNA)的基因物质.
    在休眠期,LATRNA被分成较小的基因链,被称为微型RN A,它们能阻碍激活病毒自我复制机制的蛋白质.唤醒因素导致病毒开始产生许多携带信息的名为信使RNA的基因链,这些基因链将抑制微型RNA,并最终导致自我复制系统重新启动.新产生的病毒进入三叉神经,来到最初被感染的唇部区域.三叉神经贯穿面颊,传输面部感觉.
    卡伦在新闻发布会上说,该研究为开发药物指明了方向,这些药物将激活病毒,然后杀死它.因为很难找到处于休眠期的病毒,所以激活病毒是很关键的一步.
    最近,在动物身上试验的一种新药旨在干扰让病毒处于不活跃状态的微型RNA.卡伦希望,一旦病毒被唤醒,病人可以服用已被证实对HSV1病毒有效的药物阿昔洛韦.
    卡伦说:“从原则上讲,可以激活然后杀死病人体内的所有病毒.这将使病人痊愈,而且唇疱疹以后永远不会复发.”
    这些发现也许还对杀死HSV2有用,HSV2会导致生殖器疱疹和水痘病毒.

MicroRNAs expressed by herpes simplex virus 1 during latent infection regulate viral mRNAs
Jennifer Lin Umbach1, Martha F. Kramer2, Igor Jurak2, Heather W. Karnowski1, Donald M. Coen2 & Bryan R. Cullen1
1. Department of Molecular Genetics and Microbiology and Center for Virology, Duke University Medical Center, Durham, North Caroline 27710, USA
2. Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA
Correspondence to: Bryan R. Cullen1 Correspondence and requests for materials should be addressed to B.R.C. (Email: culle002@mc.duke.edu).
Herpesviruses are characterized by their ability to maintain life-long latent infections in their animal hosts. However, the mechanisms that allow establishment and maintenance of the latent state remain poorly understood. Herpes simplex virus 1 (HSV-1) establishes latency in neurons of sensory ganglia, where the only abundant viral gene product is a non-coding RNA, the latency associated transcript (LAT)1, 2. Here we show that LAT functions as a primary microRNA (miRNA) precursor that encodes four distinct miRNAs in HSV-1 infected cells. One of these miRNAs, miR-H2-3p, is transcribed in an antisense orientation to ICP0—a viral immediate-early transcriptional activator that is important for productive HSV-1 replication and thought to have a role in reactivation from latency3. We show that miR-H2-3p is able to reduce ICP0 protein expression, but does not significantly affect ICP0 messenger RNA levels. We also identified a fifth HSV-1 miRNA in latently infected trigeminal ganglia, miR-H6, which derives from a previously unknown transcript distinct from LAT. miR-H6 shows extended seed complementarity to the mRNA encoding a second HSV-1 transcription factor, ICP4, and inhibits expression of ICP4, which is required for expression of most HSV-1 genes during productive infection4. These results may explain the reported ability of LAT to promote latency5, 6, 7, 8, 9. Thus, HSV-1 expresses at least two primary miRNA precursors in latently infected neurons that may facilitate the establishment and maintenance of viral latency by post-transcriptionally regulating viral gene expression.

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