Investigation for signals and host factors related to paramyxovirus budding.
| Project/Area Number |
15590418
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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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 | HIROSHIMA UNIVERSITY |
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Principal Investigator |
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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| Project Period (FY) |
2003 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2004: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2003: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | virus / Sendai virus / assembly / budding / virus-like particle / M protein / C protein / AIP1 / Alix / 宿主因子 |
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| Research Abstract |
In the present project, we obtained the results described below.
Firstly, we established a system to generate virus-like particles (VLPs) similar to Sendai virus (SeV) by co-transfecting multiple viral proteins. By using the system, we found that the accessory C protein had an ability to facilitate VLP release. We further demonstrated that the C protein interacted a host factor, AIP1/Alix, and that the interaction was essential for the VLP facilitation.
Secondly, we confirmed that the M protein is a driving force for the particle release from cells, and we identified a late domain motif in the M protein, which was further shown to interact with AIP1/Alix. Neither Tsg101 nor Nedd4 appeared to be involved in the M protein function, but ubiquitin and Vps4A were involved in it.
Thus, both of the M and C proteins are important for virus budding probably by interacting AIP1/Alix. The interaction was presumed to recruit the endosome-sorting complex required for transport (ESCRT) to virus budding. We further identified amino acid motifs for the interaction between the SeV proteins and AIP/Alix, and will generate viruses carrying the mutations incompetent to binding with AIP1/Alix to confirm and extend our results. As described, viral proteins important virus budding, viral protein motifs for the function, and related host factors are being clarified.
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Report
(4 results)
Research Products
(23 results)
