| Project/Area Number |
03404014
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Applied veterinary science
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| Research Institution | The university of Tokyo |
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Principal Investigator |
MIKAMI Takeshi Univ. of Tokyo, Fac. of Agr., Professor, 農学部, 教授 (20091506)
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| Co-Investigator(Kenkyū-buntansha) |
GOITSUKA Ryo Univ. of Tokyo, Fac. of Agr., Research Associate, 農学部, 助手 (60205581)
TOHYA Yukinobu Univ. of Tokyo, Fac. of Agr., Research Associate, 農学部, 助手 (20180119)
TSUJIMOTO Hajime Univ. of Tokyo, Fac. of Agr., Associate Professor, 農学部, 助教授 (60163804)
KAI Chieko Univ. of Tokyo, Fac. of Agr., Associate Professor, 農学部, 助教授 (10167330)
新倉 昌浩 東京大学, 農学部, 助手 (50212113)
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| Project Period (FY) |
1991 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥28,000,000 (Direct Cost: ¥28,000,000)
Fiscal Year 1993: ¥4,500,000 (Direct Cost: ¥4,500,000)
Fiscal Year 1992: ¥9,000,000 (Direct Cost: ¥9,000,000)
Fiscal Year 1991: ¥14,500,000 (Direct Cost: ¥14,500,000)
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| Keywords | FIV / follicular dendritic cell / feline calicivirus / feline herpesvirus type 1 / LTR / immediate early gene / ICP4 homologue / イヌジステンパーウイルス / ネコヘルペスウイルス / ネコカリキウイルス / 持続感染 / 再活性化 / 標的細胞 / イヌヘルペスウイルス |
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| Research Abstract |
In persistent infection, virus can hidden in body and escape from immunological prcsurc, in spite of the presence of immunity. However, the virus is sometimes reactivated to produce diseases in host. Following results were obtained.
The feline immunodeficiency virus (FIV) antigens were observed in many follicular dandritic cells (FDCs) and sparsely in small lymphocytes of paracortical area in the lymph nodes of cats inoculated with FIV
Feline calicivirus causes persistent infection in feline T-cells in vitro
Feline herpcsvirus type 1(FHV-1) activated FIV long terminal repeat(LTR). The target sites in LTR appeared to be ATF binding site and TATA element
The nucleotide sequence of FHV-1 immuediate early (IE) gene and its flanking sequences were identified as a ICP4 homologue of HSV-1. The sequence had ahomology of 35-50% with ICP4 homologue of other a herpesvirus
The HSV-1, PRV and EHV-1 ICP4 homologues can transrepress the FIV, while the FHV-1 ICP4 homologue has no effect in CRFK and Felis catus whole fetus 4(fcwf-4) cells. The FHV-1 ICP4 homologue can stimulate the HIV LTR in CPFK cells but not in fcwr-4 cells. The others have or little effect in CRFK and fcwf-4 cells All the ICP4 homologues can transactivate the FIV and HIV LTRs in SW480 cells.
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