1998 Fiscal Year Final Research Report Summary
Medical use of protease inhibitors for virus infection
| Project/Area Number |
09044314
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| Research Category |
Grant-in-Aid for international Scientific Research
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| Allocation Type | Single-year Grants |
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| Section | Joint Research |
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| Research Field |
Pathological medical chemistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
KIDO Hiroshi Institute for Enzyme Research, University of Tokushima, Professor, 分子酵素学研究センター, 教授 (50144978)
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| Co-Investigator(Kenkyū-buntansha) |
BODE Wolfram Max-planch-Institute fuy Biochemie, Professor, 生化学部, 教授
FRITZ Hans Dept.of clinic.Biochem.Univ.of Munich, Professor, 臨床化学生化学部, 教授
YANO Mihiro the Institute for Enzyme Research, Lecturer, 分子酵素学研究センター, 助手 (40304555)
TOWATARI Takao the Institute for Enzyme Research, University of Tokushima, assistant Professor, 分子酵素学研究センター, 助教授 (60108876)
TASHIRO Mashato Natl.Iust.of Iufectous Diseare Dept.of viral Disease, ウイルス第一部, 部長 (90111343)
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| Project Period (FY) |
1997 – 1998
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| Keywords | influenza virus / processing / tryptase Clara / plasmin / miniplasmin / antileukoprotease / elastase / urokinase |
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| Research Abstract |
Tryptase Clara, a uypsin-likc protease localized exclusively in and secreted from Clara cells of the bronchial epithielium proteolytically activates the infectivity of influenia A virus. In this rcsearch project, we found that miniplasmin as well as tryptase Clara also activates infectivity of influenza virus in vitro. Miniptasmin is formed From plasminoge n after processing by urokinase and elastase. To identify the endogenous inhibitor(s) of tryptase Clara in airway as a defensive compounds, we examined human bronchial lavage fluid and found two inhibitors of this enzyme. One was a pulmonary surfactant and the other was antilcukoprotease inhibitor (ALP). Miniplasmin was inhibited by hurnan-inter-alpha-trypsin inhibitor and urinary trypsin inhibitor but not by ALP.In this reseach, the two host proteases, tryptase Clara and miniplasrmn. and their endogerious inhibitors illustrate the role of cellular factors in the regulationof influenza virus infection.
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