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Molecular biological studies on virulence factor s and molecular pathogenesis of infectious bursal dissease virus

传染性法氏囊病病毒毒力因子及分子发病机制的分子生物学研究

基本信息

批准号：
18580308
负责人：
YAMAGUCHI Tsuyoshi
金额：
$ 2.47万
依托单位：
Tottori University (2007)Gifu University (2006)
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2006
资助国家：
日本
起止时间：
2006 至 2007
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18580308/
关键词：
Infectious bursal disease virus virulence apoptosis cytotoxicity nonstructural protein microarray subcellular localization VP5 VP2

项目摘要

In the present study, to understand the molecular mechanism for the virulence or pathogenicity of the virulent infectious bursal disease virus (IBDV), several experiments were employed as listed below.1. Usefulness of chicken B lymphoma LSCC-DT40 cell as a tool for in vitro analysis of virulent IBDV was examined. Although freshly isolated virulent IBDV doesn't propagate in chicken embryo fibroblast cell without adaptation, the virulent IBDV easily propagate in DT40 cell. This findings indicate the usefulness of the cell for in vitro analysis of the virulent IBDV.2. Cytotoxicity and subcellular localization of viral proteins of virulent IBDV was examined. Transient expression of VP4 derived from virulent IBDV localized in nucleus and is apoptotic to the host cell. Furthermore, it was revealed that palmitoylation of VP5 is important for the localization of VP5 at plasma membrane, which is known as essential event for cell lysis observed in IBDV infection.3. Microarray analysis of host cell gene transcription in response to virulent IBDV infection of DT40 was examimned. Transcriptional change in 170 genes of DT40 cell was found after virulent IBDV infection. Different transcriptional changes were found depend on the virulence of IBDV.4. IBDV infection resistant DT40 cell was established and the transcriptional profiles were examined. Thousands of significant changes were found in the transcription between IBDV susceptible and resistant DT40 cells.

在本研究中，为了了解强毒传染性法氏囊病病毒（IBDV）的毒力或致病性的分子机制，进行了以下几项实验。研究了鸡B淋巴瘤LSCC-DT40细胞作为体外毒力IBDV检测工具的有效性。虽然新分离的强毒IBDV在鸡胚成纤维细胞中没有适应，但在DT40细胞中很容易繁殖。这一发现表明该细胞可用于体外毒力ibdv的分析。研究了强毒IBDV病毒蛋白的细胞毒性和亚细胞定位。由毒力强的IBDV衍生的VP4在细胞核内的瞬时表达，并导致宿主细胞凋亡。此外，我们还发现VP5的棕榈酰化对于VP5在质膜上的定位很重要，这是IBDV感染中观察到的细胞裂解的必要事件。采用微阵列分析方法研究了宿主细胞基因转录对强毒IBDV感染DT40的反应。在IBDV强毒感染后，发现DT40细胞有170个基因发生了转录变化。发现不同的转录变化取决于ibdv的毒力。建立了抗IBDV感染的DT40细胞，并检测了转录谱。在IBDV易感和耐药的DT40细胞之间发现了数千个显著的转录变化。