| Project/Area Number |
01480181
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Virology
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| Research Institution | Nagoya University |
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Principal Investigator |
NAGAI Yoshiyuki Nagoya University School of Medicine, Professor, 医学部, 教授 (20022874)
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| Co-Investigator(Kenkyū-buntansha) |
HAMAGUCHI Michinari Nagoya University School of Medicine, Associate Professor, 医学部, 助教授 (90135351)
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥6,700,000 (Direct Cost: ¥6,700,000)
Fiscal Year 1990: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 1989: ¥4,000,000 (Direct Cost: ¥4,000,000)
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| Keywords | Factor X / Fusion glycoprotein / Paramyxovirus / Orthomyxovirus / Proteolytic activation / Viral tropism / ウイルス臓器向性 / ミクソウイルス / プロテア-ゼ / 血液凝固第10因子 |
|---|
| Research Abstract |
Host cell proteases responsible for activation of viral fusion glycoproteins are an important determinant for spread and tropism of various animal viruses. Exemplifying such proteases for the first time, we isolated an endoprotease from chick embryo that activates para- and orthomyxovirus fusion glycoproteins by cleaving their precursor proteins at a specific, single arginine-containing site. The protease is a calcium dependent serine protease consisting of two subunits, the 33 Kd catalytic chain and the 23 Kd chain possibly required for Ca^<+2> binding, and was found to be highly homologous, if not identical, to the blood clotting factor X (FX), a member of the prothrombin family. Its high efficiency and specificity 1 in cleavage reaction were attributable to the properties characteristic of FX. Its role in vivo was strongly supported by cleavage inhibition in ovo highly selective for this virus group with a specific peptide inhibitor against FX. We have further prepared specific cDNA and antibody probes for FX and are now investigating the expression of FX gene in each tissue of the whole embryo. The preliminary results obtained by these studies strongly suggested that the ectopic expression of FX is the sole determinant for the viral tropism in the embryo.
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