| Project/Area Number |
26860277
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Parasitology (including sanitary zoology)
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| Research Institution | Chiba University (2015)
Teikyo University (2014) |
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Principal Investigator |
Hikosaka Kenji 千葉大学, 医学(系)研究科(研究院), 特任助教 (30456933)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | マラリア / Plasmodium / 薬剤耐性 / 抗マラリア薬 / アトバコン / ミトコンドリアゲノム / 動物感染モデル |
|---|
| Outline of Final Research Achievements |
To clarify mechanism of emergence of resistance to antimalarial drugs, we investigated emergence patterns of a point mutation associated with drug resistance using Plasmodium berghei-infected mice. In this study, atovaquone (ATQ), targeting cytochrome b (cob) gene encoded on mitochondrial DNA (mtDNA) of Plasmodium, was selected as an antimalarial drug. In a result, four non-synonymous mutations were found in cob; three mutations (L271V、K272R and V284F) were already reported and the remaining one (I258M) was new. In order to further elucidate emergence patterns of these point mutations, we performed deep sequencing of Plasmodium mtDNA, which was extracted from infected blood collected continuously, using a next-generation sequencer. Analysis of the deep sequencing revealed that the mutation (V284F) was dramatically emerged six days after administration of ATQ. In the future, we will investigate emergence pattern of the other mutations (L271V、K272R and I258M) by deep sequencing.
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