2011 Fiscal Year Final Research Report
Analysis for the molecular basis of rabies virus pathogenicity following peripheral infection
| Project/Area Number |
21780278
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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 |
Applied veterinary science
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| Research Institution | Oita University |
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Principal Investigator |
YAMADA Kentaro 大分大学, 全学研究推進機構, 助教 (70458280)
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| Project Period (FY) |
2009 – 2011
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| Keywords | 狂犬病 / 狂犬病ウイルス / 街上毒 / 末梢感染 / 病原性 / N型糖鎖 |
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| Research Abstract |
It is still unclear how rabies viruses enter into the central nervous system from a bite site and then cause rabies. In this study, by serial passaging of the street rabies virus strain 1088 in a neuroblastoma cell line, we established a variant that was attenuated in mice following i. m. but not i. c. infections. We found that addition of an N-glycan to the viral G protein is related to the attenuation. Concerning the additional N-glycosylation is also found in laboratory-adapted strains but not street strains, the N-glycosylation status of the G protein is probably one of the determinants for the rabies virus pathogenicity following peripheral infection.
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[Journal Article] Serial passage of a street rabies virus in mouse neuroblastoma cells resulted in attenuation : Potential role of the additional N-glycosylation of a viral glycoprotein in the reduced pathogenicity of street rabies virus2012
Author(s)
Yamada K., Park C. H., Noguchi K., Kojima D., Kubo T., Komiya N., Matsumoto T., Mitui M. T., Ahmed K., Morimoto K., Inoue S., Nishizono A.
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Journal Title
Virus Research
Volume: 165巻, 1号
Pages: 34-45
Peer Reviewed
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