| Co-Investigator(Kenkyū-buntansha) |
KIYOTANI Katsuhiro Hiroshima University, Graduate School of Biomedical Sciences, Assistant Professor, 大学院・医歯薬学総合研究科, 講師 (00106824)
SAKAGUCHI Takemasa Hiroshima University, Graduate School of Biomedical Sciences, Associate Professor, 大学院・医歯薬学総合研究科, 助教授 (70196070)
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| Budget Amount *help |
¥5,400,000 (Direct Cost : ¥5,400,000)
Fiscal Year 2003 : ¥1,300,000 (Direct Cost : ¥1,300,000)
Fiscal Year 2002 : ¥1,500,000 (Direct Cost : ¥1,500,000)
Fiscal Year 2001 : ¥2,600,000 (Direct Cost : ¥2,600,000)
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| Research Abstract |
Sendai virus (SeV) is a paramyxovirus causing bronchopneumonitis in rodents and possesses a nonsegmented single-stranded minus-sense RNA as a genome. In the present study we examined the function of SeV accessory V protein and the attenuation of SeV pathogenicity by egg passages to study the regulation of SeV gene expression and pathogenesis by host factors, and the following results were obtained.
(1) The V protein of the Hamamatsu strain, a highly virulent field SeV isolate, has been shown to have a luxury function to facilitate virus propagation in mice but not in cultured cells as well as that of the Z strain, an egg-adapted avirulent laboratory SeV strain, and to be prominent only if virus replication was restricted. (ref. 4, 8, 14, and 17)
(2) The luxuary function of the V protein has been shown to be dependent on the amino acid residues at the C terminus of the protein, which are highly conserved among paramyxoviruses, probably via protein conformation dependent on Zn binding. (ref. 1, 4, 8, and 13)
(3) The V protein function, probably by coping with the host innate immunity, antagonized neither interferon action nor NK cell activity. The cellular target of the V protein remains to be clarified. (ref. 17, unpublished data)
(4) Attenuation of SeV pathogenicity by egg passages has been shown to be caused at least by mutations of the nucleotides at position 20 and 24 in the leader sequence, suggesting that the leader mutaions affect virus pathogenesis by altering virus replication via interaction with host factors. (ref. 6, 12, and 14)
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