| Project/Area Number |
17K15366
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Veterinary medical science
|
|---|
| Research Institution | Hokkaido University |
|---|
Principal Investigator |
Hayashida Kyoko 北海道大学, 人獣共通感染症リサーチセンター, 特任助教 (40615514)
|
|---|
| Project Period (FY) |
2017-04-01 – 2020-03-31
|
| Project Status |
Completed (Fiscal Year 2019)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
|---|
| Keywords | トリパノソーマ原虫 / 進化 / ゲノム / 人獣共通感染症 / アフリカトリパノソーマ / Trypanosoma evansi / スーラ / ズーノーシス / 分子進化 / トリパノソーマ / 血清抵抗性 / トランスクリプトーム / 野外分離株 |
|---|
| Outline of Final Research Achievements |
Human had evolved to acquire the natural immunity against Trypanosoma infection, called Trypanolytic factor (TLF) in its serum. On the other hand, two Trypanosome species evolved to acquire the mechanism to combat with human anti-Trypanosome immune system, allowing to infect humans. To better understand of host-parasite interaction of the Trypanozoon parasite, we adapted T. evansi parasite into human-serum added media in vitro. Genome-wide transcription analysis using RNA-seq revealed that, several genes are differentially expressed comparing the original strain in these human-serum resistant parasite clones. Notably, the expression of HpHbR gene, that encodes the parasite receptor of TLF was significantly downregulated. This result provided a possible mechanism of African Trypanosoma to acquire human serum resistance, and proposed the potential risk of animal-infective Trypanosoma to become an potential zoonotic parasite.
|
| Academic Significance and Societal Importance of the Research Achievements |
ヒトのアフリカ睡眠病を引き起こすTrypanosoma brucei と、家畜の病原体であるT. evansiは近縁関係にあるが後者はヒト血清抵抗性を有さない。本研究ではT. evansiを試験管内でヒト血清へ馴化し網羅的遺伝子解析を行った。結果、ヒトの抗トリパノソーマ因子TLFのレセプターHpHbRの発現が血清抵抗性T. evansiで減少していることを明らかにした。本知見はヒト血清抵抗性の獲得という現象が、Trypanozoon亜属に共通して起こりうる現象であることを示唆する。T. evansiが新たな人獣共通感染症の原因となりうるのか、今後慎重に検討すべき課題であると考えられる。
|
