| Project/Area Number |
12670273
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Virology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
WATANABE Shinya The University of Tokyo, Institute of Medical Science, Research associate, 医科学研究所, 助手 (70251444)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2001: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2000: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | cytomegalovirus / microarray / host cell factors / DNAマイクロアレイ |
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| Research Abstract |
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.
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