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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.

人巨细胞病毒（HCMV）在正常人成纤维细胞中有效复制，但在大多数永生化细胞系中复制有限或很少。为了研究 HCMV 征服并控制成纤维细胞以实现病毒成功繁殖的分子策略，我们使用微阵列系统分析了 HCMV 感染细胞的转录组，该系统具有代表 NCBI RefSeq 数据库中 9,600 个人类命名基因的合成多核苷酸。我们编译了从 wile 型 HCMV 感染和 UV 灭活的 HCMV 感染的成纤维细胞以及接种受感染细胞培养基的成纤维细胞获得的表达谱，发现 HCMV 通过病毒颗粒的吸附和/或渗透以及随后通过初始事件后细胞外分泌的因子引发广泛的细胞反应。此外，野生型和紫外线灭活病毒感染细胞之间转录组的比较表明，HCMV最终通过在病毒复制周期中从头合成的病毒基因产物来抑制负责抵抗外源刺激的细胞基因的表达。这些结果表明，对主要参与炎症的细胞负责基因的抑制可能表明宿主细胞总体上服从于病毒。