| Project/Area Number |
10470082
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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 |
Virology
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| Research Institution | Nagoya City University |
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Principal Investigator |
NAKAJIMA Katsuhisa Nagoya city University, Medical School, Professor, 医学部, 教授 (40012778)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAJIMA Setsuko Institute of Public Health, Dep.Microbiol.Section Chief, 微生物学部, 室長 (80124402)
IIDUKA Narusi Nagoya City University, Medical School, Research Associate, 医学部, 助手 (30222821)
NOBUSAWA Eri Nagoya City University, Medical School, Associate Professor, 医学部, 助教授 (90183904)
小塚 諭 名古屋市立大学, 医学部, 助手 (40117817)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥13,200,000 (Direct Cost: ¥13,200,000)
Fiscal Year 2000: ¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 1999: ¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1998: ¥6,600,000 (Direct Cost: ¥6,600,000)
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| Keywords | Influenza virus / virion formation / HA protein / neuraminidase / desialidation / GG167 / インフルエンザウィルス |
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| Research Abstract |
We analyzed the role of neuraminidase (NA) on the haemadsorption of haemagglutinin (HA) protein of influenza B virus. The influenza B virus mutant ts-7 had temperature-sensitive mutation in the NA protein. At high temperature, infected cells did not exhibit haemadsorption activity, but addition of bacterial neuraminidase restored haemadsorption activity. Experiments with point-mutated HA cDNAs of B virus showed that two N-acetyl glycosylation sites at amino acid residues 160 and 217 were responsible for the inability of the HA protein to adsorb to erythrocytes. These results indicated that haemadsorption by the HA protein of influenza B virus required involvement of neuraminidase. Because the neuraminidase inhibitor Zanamivir was reported not to penetrate cells, we investigated the action of this inhibitor and found that Zanamivir inhibited haemadsorption on MDCK cells infected with B virus. These results indicated that desialidation of HA was done by NA after two proteins moved to cel
… More
l surface. From the reassortment experiments between A/Aichi/92 and A/WSN/33 (WSN) viruses, two different phenotype viruses which contained HA gene from A/Aichi/ 92 virus and the NA gene from WSN virus were obtained. PW15 viruse agglutinated chicken red blood cells (CRBC), while PW10 virus did not. However, the expressed HA proteins of these viruses did not adsorb CRBC.The difference in gene constellation between PW15 and PW10 viruses was the membrane protein (M) gene. The former had the M gene from A/Aichi/4/92 virus and the latter had that from WSN virus. In PW15-infected cells, haemadsorption of CRBC was observed 30 min later than that of goose red blood cells and the M1 protein migrated from the nucleus to the cytoplasm 30 min earlier than adsorption of CRBC was observed. On the other hand, in PW1O-infected cells, haemadsorption of CRBC was not observed through the virus replication and the M1 protein stayed in the nucleus after HA and NA activities reached maximum levels. Therefore M1 protein may contribute the desialidation of HA protein by NA protein. Less
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