...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Viruses >Herpes Simplex Virus Type 1–Encoded miR-H2-3p Manipulates Cytosolic DNA–Stimulated Antiviral Innate Immune Response by Targeting DDX41
【24h】

Herpes Simplex Virus Type 1–Encoded miR-H2-3p Manipulates Cytosolic DNA–Stimulated Antiviral Innate Immune Response by Targeting DDX41

机译：1型单纯疱疹病毒编码的miR-H2-3p通过靶向DDX41操纵胞质DNA刺激的抗病毒先天免疫反应。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Herpes simplex virus type 1 (HSV-1), one of the human pathogens widely epidemic and transmitted among various groups of people in the world, often causes symptoms known as oral herpes or lifelong asymptomatic infection. HSV-1 employs many sophisticated strategies to escape host antiviral immune response based on its multiple coding proteins. However, the functions involved in the immune evasion of miRNAs encoded by HSV-1 during lytic (productive) infection remain poorly studied. Dual-luciferase reporter gene assay and bioinformatics revealed that Asp-Glu-Ala-Asp (DEAD)-box helicase 41 (DDX41), a cytosolic DNA sensor of the DNA-sensing pathway, was a putative direct target gene of HSV-1-encoded miR-H2-3p. The transfection of miR-H2-3p mimics inhibited the expression of DDX41 at the level of mRNA and protein, as well as the expression of interferon beta (IFN-β) and myxoma resistance protein I (MxI) induced by HSV-1 infection in THP-1 cells, and promoted the viral replication and its gene transcription. However, the transfection of miR-H2-3p inhibitor showed opposite effects. This finding indicated that HSV-1-encoded miR-H2-3p attenuated cytosolic DNA–stimulated antiviral immune response by manipulating host DNA sensor molecular DDX41 to enhance virus replication in cultured cells.
机译：1型单纯疱疹病毒（HSV-1）是广泛传播并在世界各地不同人群之间传播的人类病原体之一，通常会引起称为口腔疱疹或终身无症状感染的症状。 HSV-1基于其多种编码蛋白，采用了许多复杂的策略来逃避宿主抗病毒免疫应答。然而，在溶血性（生产性）感染过程中，HSV-1编码的miRNA的免疫逃逸所涉及的功能仍然研究不足。双荧光素酶报告基因基因检测和生物信息学研究表明，Asp-Glu-Ala-Asp（DEAD）盒解旋酶41（DDX41）是DNA传感途径的胞质DNA传感器，是HSV-1-的假定直接靶基因。编码的miR-H2-3p。转染miR-H2-3p模拟物可抑制DDX41在mRNA和蛋白水平上的表达，以及HSV-1感染诱导的干扰素β（IFN-β）和粘液抵抗蛋白I（MxI）的表达。 THP-1细胞，并促进了病毒复制及其基因转录。但是，miR-H2-3p抑制剂的转染显示相反的作用。这一发现表明，HSV-1编码的miR-H2-3p通过操纵宿主DNA传感器分子DDX41来增强在培养细胞中的病毒复制，从而减弱了胞质DNA刺激的抗病毒免疫应答。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号