| Project/Area Number |
07456133
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Basic veterinary science/Basic zootechnical science
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| Research Institution | The University of Tokyo |
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Principal Investigator |
OTSUKA Haruki Graduate School of Agriculture and Life Sciences, The University of Tokyo, Professor, 大学院・農学生命科学研究科, 教授 (80261957)
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| Co-Investigator(Kenkyū-buntansha) |
THOYA Yukinobu Faculty of Agriculture, Kagoshima University, Associate Professor, 農学部, 助教授 (20180119)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥7,100,000 (Direct Cost: ¥7,100,000)
Fiscal Year 1996: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1995: ¥5,100,000 (Direct Cost: ¥5,100,000)
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| Keywords | Herpesvirus / host range / BHV-1 / PRV / glycoprotein / thymidine kinase / CHV / FHV-1 / チミジンキナーゼ / FHV-1 |
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| Research Abstract |
Bovine herpesvirus-1 (BHV-1) can replicate well in bovine-derived cell lines such as MDBK,but grows poorly in Hamster Lung fibroblast (HmLu-1). In order to gain some insight into the molecular basis for cell tropism of herpesvirus, we investigated the expression and function of BICP4, the major regulatory protein of BHV-1, in permissive MDBK and non-permissive HmLu-1 cells. When HmLu-1 cells were infected with BHV-1 at a high multiplicity of infection, less than 20% of the infected population expressed BICP4. On the other hand almost 100% of BHV-1 infected MDBK cells express BICP4. Western blot analyzes of BHV-1 infected MDBK cells indicated that at least three major bands with molecular weights of 160,190 and 200 kDa reacted with anti-BICP4 serum. The 160 and 200 kDa bands of BICP4 was detected in BHV-1 infected HmLu-1 cells but the 190 kDa band was missing. Furthermore, induction of BICP4 in HmLu-1 cells was much more delayd than in MDBK cells. The transient and recombinant CAT assay for the BHV-1 promoters revealed that BICP4 produced in BHV-1 infected HmLu-1 cells activated the early and late promoters, indicating that BICP4 was functional in non-permissive HmLu-1 cells. Our results indicated that the growth of BHV-1 in non-permissive HmLu-1 was restricted at the level of the transcription of the immediate early (IE) genes and that only a small fraction of infected population transcribed the IE genes at a low level, eventually producing a small number of infectious virus particles in this population of cells.
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