罗敏华教授学术报告

 题  目：Neuropathy Induced by Human Cytomegalovirus Infection

报告人：罗敏华 研究员  中国科学院武汉病毒研究所

时  间：8月13日，周三，下午2：00

地  点：科B502

报告摘要：

Congenital human cytomegalovirus (HCMV) infection is a leading cause of birth defects, primarily neurological disorders. There are two kinds of clinic manifestations, including being symptomatic at birth (microencephaly), and late on-set sequelae (sensorineural hearing loss (SNHL)). To study the neuropathy, we need to establish the human neural cell models accordingly. We have established HCMV productive infection NPCs model and persistent/latent infection T98G cell model. It has been found that NPCs and the derivates are fully permissive for HCMV infection, induced neural cell loss and abnormal differentiation by HCMV (J Vi 2008, 2010, 2013; ABBS 2012). In the persistent/latent infected T98G cell model, high copy number of HCMV genomes are maintained and lasted T98G cells, which is valuable for HCMV latency study (J Vi, 2007, 2014). Recently we demonstrate that mature miR-21 is repressed and CDC25a is activated during infection of NPCs and U-251 MG cells. The opposing impact on miR-21 and CDC25a prompted an investigation of the relationship of these cellular gene products and HCMV infection. Over expression of miR-21 by lentiviral transduction of NPCs and U-251 MG cells inhibited viral gene expression, genome replication, and production of infectious progeny, while knockdown of miR-21 by shRNA increased viral gene expression. In contrast, over expression of CDC25a increased viral gene expression and production of infectious progeny in U-251 MG cells and overcame the inhibitory effects of miR-21 over expression. These results suggest that Cdc25a promotes HCMV replication and that elevation of Cdc25a levels post HCMV infection are due in part to HCMV-mediated repression of miR-21. Thus, miR-21 is an intrinsic antiviral factor and modulation of miR-21 may have potential clinical applications.

报告人简介：

        罗敏华，医学博士，研究员 （百人计划）。中国科学院武汉病毒研究所神经病毒学组组长，分子病毒室副主任，美国爱达荷大学客座助理教授(assistant professor)。在湖南医科大学完成本科（临床医学）、硕士（微生物学）、博士（传染病学）学习。 主要从事人巨细胞病毒（HCMV）感染致胎儿神经发育畸形研究。主要成果：1) 首次建立了HCMV容许性感染的神经干细胞模型,发现HCMV感染直接导致神经损伤和诱导神经干细胞异常分化，部分解析了HCMV感染致脑损伤机制。2) 建立了HCMV持续/潜伏感染的神经细胞模型，发现高拷贝HCMV基因组持续存留于细胞中，为HCMV持续/潜伏感染这一关键科学问题的深入研究提供了首个神经细胞模型。3) 建立了HCMV网络宣传教育平台。近5年在病毒学顶级杂志Journal of Virology 上发表论文7篇，部分成果成为Journal of Virology 亮点。目前承担中国科学院“百人计划”、中国科学院外国专家特聘研究员计划、国家自然科学基金、“973”计划等多项国家科研项目，参与“脑功能联结图谱计划”和“多能干细胞研究免疫学基础” 中国科学院战略先导科技专项。

       课题组主要进行病毒学和神经科学交叉领域研究：1.HCMV在神经系统中的潜伏与激活机制；2.HCMV感染对神经干细胞增殖和分化的影响及其机制。3.改造嗜神经病毒，为神经回路示踪和脑联结研究提供新的有效的示踪工具，解析工具病毒跨突触传播机制和神经疾病机制。