Project/Area Number |
09470083
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Virology
|
Research Institution | Nagoya University |
Principal Investigator |
NISHIYAMA Yukihiro Nagoya University, School of Medicine, Professor, 医学部, 教授 (60115615)
|
Co-Investigator(Kenkyū-buntansha) |
DAIKOKU Tohru School of Medicine, Research Associate, 医学部, 助手 (80291409)
GOSHIMA Fumi School of Medicine, Research Associate, 医学部, 助手 (70201499)
|
Project Period (FY) |
1997 – 1999
|
Project Status |
Completed (Fiscal Year 1999)
|
Budget Amount *help |
¥11,800,000 (Direct Cost: ¥11,800,000)
Fiscal Year 1999: ¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 1998: ¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1997: ¥5,300,000 (Direct Cost: ¥5,300,000)
|
Keywords | herpes simplex virus / accessory gene / function of viral proteins / protein kinase / mechanism of viral replication / 非必須遺伝子 / US3 / アポトーシス |
Research Abstract |
We have constructed prokaryotic and eukaryotic expression vectors of herpes simplex virus type 2 (HSV-2) genes, generated rabbit polyclonal antibodies against fusion proteins expressed in Escherichia coli, and then identified a number of HSV-2 gene products including UL3, UL4, UL14, UL16, UL17, UL31, UL51, UL55, and US2. All of them were produced at the late phase of infection : properties of some of them are summarized as follows. ・The UL4 gene product was identified as a 27-kDa protein in infected cells. Indirect immunofluorescence studies localized the UL14 protein within the nucleus as discrete punctate forms at late times postinfection, but the protein was limited to the cytoplasm when expressed alone, indicating that an interaction with one or more other virus-induced proteins was responsible for the nuclear localization during infection. ・The UL16 gene product was identified as a 41-kDa protein in infected cells, and produced in a manner highly dependent on viral DNA synthesis. The UL16 protein was distributed in both the nuclei and the cytoplasm, and was associated with intracellular C capsids. Our results suggest that the UL16 protein plays a role in capsid maturation including DNA packaging/cleavage. We have also studied the biological role of the US3 gene product in a murine model of HSV infection, and found that the US3 protein kinase plays an important role in protecting HSV-2-infected cells from apoptotic death in vivo.
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