Identification or cellular factors associated with cytomegalovirus replication by cDNA microarrays

通过 cDNA 微阵列鉴定与巨细胞病毒复制相关的细胞因子

基本信息

批准号：
12670273
负责人：
WATANABE Shinya
金额：
$ 2.18万
依托单位：
The University of Tokyo
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2000
资助国家：
日本
起止时间：
2000 至 2001
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-12670273/
关键词：
cytomegalovirus microarray host cell factors DNAマイクロアレイ

项目摘要

Human cytomegalovirus (HCMV) replicates efficiently in normal human fibroblasts but restrictedly or scarcely in most immortalized cell lines. To investigate a molecular strategy under which HCMV conquests and governs the permissive fibroblasts toward succeeding virus propagation, we analyzed transcriptomes for HCMV-infected cells using a microarray system with synthetic polynucleotides representing 9,600 of human named genes in the RefSeq database of NCBI. We compiled expression profiles obtained from wile-type HCMV-ingected and UV-inactivated HCMV-infected fibroblasts as well as fibroblasts inoculated with culture media of the infected cells and found that HCMV elicits a wide range of cellular responses via adsorption and/or penetration of viral particles and subsequently via factors exrtracellularly secreted after the initial events. Moreover, comparison of the transcriptomes between wild type and UV-inactivated virus-infected cells revealed that HCMV eventually suppresses expression of the cellular genes which are responsible against exogenous stimuli by means of viral gene products synthesized de novo during the viral replication cycle. These results suggest that suppression of the cellular responsible genes mostly involved in inflammation may indicate the overall submission to of the host cell to the virus.

人类巨细胞病毒（HCMV）在正常的人成纤维细胞中有效地复制，但在大多数永生的细胞系中受到限制或几乎不受限制。为了研究一种分子策略，在该策略下，HCMV征服并控制了允许的成纤维细胞用于成功病毒传播的允许性成纤维细胞，我们使用具有合成多核苷酸的微阵列系统分析了HCMV感染的细胞的转录组，该系统代表了NCBBI的REFSEQ数据库中的人为基因的9,600基因。我们收集了从Wile型HCMV诱导和紫外线灭活的HCMV感染的成纤维细胞以及与感染细胞的培养基接种的成纤维细胞获得的表达曲线，并发现HCMV发现HCMV通过吸附和/或/或渗透而引起了HCMV的广泛细胞反应。初始事件后，病毒颗粒，随后通过extracellachiles分泌的因素。此外，比较野生型和紫外线灭活病毒感染的细胞之间的转录组表明，HCMV最终抑制了通过病毒复制周期中病毒基因产物从从头开始的病毒基因产物对外源刺激负责的细胞基因的表达。这些结果表明，主要参与炎症的细胞负责基因的抑制可能表明宿主细胞对病毒的总体提及。