| Project/Area Number |
07807037
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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 | National Institute of Health |
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Principal Investigator |
ARAO Yujiro National Institute of Health, Dept. of Pathology, Senior Researcher, 感染病理部, 主任研究官 (40151146)
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| Co-Investigator(Kenkyū-buntansha) |
ANDO Yasutaka Keio University Medical School, Dept. of Ophtalmology, Researcher, 医学部・眼科学教室, 助手 (90193119)
IWASAKI Takuya National Institute of Health, Dept. of Pathology, Chief Researcher, 感染病理部, 室長 (90146027)
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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 |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1996: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1995: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | Herpes simplex virus type 1 / Herpes simplex virus type 2 / Human interferon alpha / Human interferon beta / Human interferon gamma / interferon resistance / Intertypic recombinant virus / Marker rescue |
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| Research Abstract |
To better understand how herpes simplex virus (HSV) counteracts anti-HSV effects of interferons (IFNs), first, the sensitivity of 19 HSV strains to type I and II IFNs was compared in the infection processes of cultured human epithelial cells. There was good correlation between the sensitivities to the IFNs although they have different anti-HSV actions. This correlation was not due to induction of endogenous type I IFN by type II IFN treatment, because a neutralizing antibody to IFN beta did not diminish the anti-HSV effects of type II IFN.A similar correlation also was observed in human embryonic lung fibroblast cells. These results suggest that HSV has an ability to overcome the anti-HSV actions of both types of IFNs independently but with similar sensitivity.
Secomd, we examined complementation and recombination between two interferon (IFN) sensitive strains, 17syn of herpes simplex virus type 1 [HSV-1 (17syn)] and UW268 of HSV type 2 [HSV-2 (UW268)]. Double infection with the two str
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ains resists reduction in virus yield by IFN.Intertypic recombinants with restored IFN resistance were obtained from progeny viruses in the doubly-infected cultures. These results indicate that IFN resistance of HSV is controlled by at least two genetic regions.
Third, restriction endonuclease analysis of the intertypic recombinants deduced that one of the HSV coding regions for IFN resistance locates in BamHI-A,BglII-N or the neighboring fragments of HSV-2. Four cloned fragments, Bam HI-A and-E and BglII-I and-N,of an IFN resistant HSV-2 strain, G[HSV-2 (G)] were tested for their abilities to rescue IFN resistance of HSV-2 (UW268), resulting in that only BglII-N incresed plating efficiency of progeny viruses in co-transfected cultures. An IFN resistant HSV-2 clone was obtained from the co-transfected culture with BglII-N of HSV-2 (G) and the HSV-2 clone contained a DNA sequence within the fragment. Therefore, it is concluded that one of the HSV coding regions for IFN resistance locates in the BglII-N fragment of HSV-2. Less
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