| Project/Area Number |
22790953
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Infectious disease medicine
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| Research Institution | Osaka University |
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Principal Investigator |
DAIDOJI Tomo 大阪大学, 微生物病研究所, 特任助教 (80432433)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 高病原性鳥インフルエンザ / 高病原性インフルエンザウイルス / アポトーシス |
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| Research Abstract |
In recent years, the highly pathogenic avian influenza virus H5N1 has raised serious worldwide concern about an influenza pandemic ; however, the mechanism of H5N1 pathogenesis is largely unknown. A/ Crow/ Kyoto/ 53/ 2004(H5N1)[ Cr/ Ky(H5N1)] showed high mortality and weight loss toward mice, while A/ Duck/ Hong Kong/ 820/ 80(H5N3) did not. In addition, recombinant H5N3 viruses carrying the H5N1 HA gene(rH5N3H5N1HA) showed the similar result with that of Cr/ Ky(H5N1). In addition, Cr/ Ky(H5N1) and rH5N3H5N1HA also indicated efficient viral replication and lung hemorrhage including inflammatory cell infiltration. The levels of proinflammatory cytokine in mice infected with rH5N3H5N1HA was higher than mice infected with Dk/ Hk(H5N3). Taken together, these data suggest that H5N1HA broaden the viral pathogenesis in mice and this pathogenesis is based on viral replication and proinflammatory cytokine balance in mice.
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