2021 Fiscal Year Final Research Report
Mechanism of attenuated SFTSV strain for live vaccine establishment
Project/Area Number |
20K17478
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Research Category |
Grant-in-Aid for Early-Career Scientists
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Allocation Type | Multi-year Fund |
Review Section |
Basic Section 54030:Infectious disease medicine-related
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Research Institution | National Institute of Infectious Diseases |
Principal Investigator |
Park Eunsil 国立感染症研究所, 獣医科学部, 主任研究官 (90750117)
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Project Period (FY) |
2020-04-01 – 2022-03-31
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Keywords | SFTSV / Reverse genetics / 弱毒株 / M分節 / GPC遺伝子 |
Outline of Final Research Achievements |
The difference of pathogenicity between attenuated strain (Cat#1) and virulent strain (SPL010) of severe fever with thrombocytopenia syndrome virus (SFTSV) has been shown through animal studies. In this study, the cause of the difference of pathogenicity was explored in the level of virus genome. Chimera virus (rgSFTSV) consisting of S, M, L segment of Cat#1 and SPL010 was prepared by reverse genetics. All of IFNAR1 knockout mouse (IFNAR1-/-) infected with rgSFTSV containing M segment of Cat#1 were survived, showing a survival rate of 100%. All of IFNAR1-/- infected with rgSFTSV containing M segment of SPL010 were dead, showing a survival rate of 0%. As a result, it is thought that M segment of SFTSV is involved in the pathogenicity.
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Free Research Field |
人獣共通感染症、ウイルス
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Academic Significance and Societal Importance of the Research Achievements |
弱毒株と強毒株の病原性にはSFTSVのM分節、GPC遺伝子が関与していることが示唆された。GPC遺伝子は膜蛋白質をコードし、宿主の受容体に結合する際に重要な役割を果たす。二つの株のM分節には18ヵ所アミノ酸が異なり、Cat#1株の18ヵ所アミノ酸をそれぞれSPL010株へ置換したrgSFTSVを作製した。現在、感染実験を通じて、原因遺伝子を解明する予定である。原因遺伝子が解明できれば、中和抗体等ウイルスに対する免疫を誘導する弱毒化生ワクチンへの応用が可能になる。
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