ANALYSIS OF MATURATION AND EGRESS OF HUMAN HERPES VIRUSES
Project/Area Number |
17390134
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Virology
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Research Institution | NATIONAL INSTITUTE OF BIOMEDICAL INNOVATION |
Principal Investigator |
MORI Yasuko NATIONAL INSTITUTE OF BIOMEDICAL INNOVATION, VIROLOGY AND VACCINOLOGY, CHIEF, 基盤研究部感染制御プロジェクト, チーフプロジェクトリーダー (50343257)
|
Project Period (FY) |
2005 – 2006
|
Project Status |
Completed (Fiscal Year 2006)
|
Budget Amount *help |
¥14,700,000 (Direct Cost: ¥14,700,000)
Fiscal Year 2006: ¥5,300,000 (Direct Cost: ¥5,300,000)
Fiscal Year 2005: ¥9,400,000 (Direct Cost: ¥9,400,000)
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Keywords | HUMAN HERPESVIRUS / INFECTION / GLYCOPROTEIN / GENE / VIRION / ウイルス / ヘルペスウイルス / HHV-6 / HHV-7 |
Research Abstract |
We analyzed the characterization of human herpesviruses in infected cells, and we got the results. The results are shown below ; 1.Human herpesvirus 6 (HHV-6) envelope cholesterol was found to be required for virus entry, especially fusion process in entry. The result also indicates that the envelope cholesterol possibly plays an important role for virus maturation as well as entry process. 2.Human herpesvirus 7 (HHV-7) encoded U47 proteins whose sizes were 49 and 51kDa, were digested with endo H and endo F, and incorporated into virions, indicating that U47 gene products are envelope glycoproteins modified with N-linked oligosaccharides. Furthermore, U47 proteins interacted with gH and gL in infected cells, indicating that U47 proteins may play roles for entry, virion maturation or egress process. 3.HHV-7 encodes two functional chemokine receptors in the U12 and U51 genes. The cellular ligands for these receptors are, respectively, MDC/CCL22 (the ligand for CCR4), and ELC/CCL19 (the ligand for CCR7). The mouse cells co-expressing CCR4 or CCR7 and U12 responded to both MDC/CCL22 and ELC/CCL19 in a calcium mobilization assay. The similar results were obtained with mouse cells co-expressing CCR4 or CCR7 with U51. These results suggest that the HHV-7 U12 and U51 receptors can function in concert with CCR4 and 12 CCR7 in host cell signaling pathways. 4.HHV-7 infection caused elevation of CRPs, CD46 and CD59, which may be a possible mechanism for HHV-7 to evade humoral immunity via complement.
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Report
(3 results)
Research Products
(8 results)