Characterization of HIV-1 latently-infected fibrocytes
Project/Area Number |
17H04221
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Infectious disease medicine
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Research Institution | Kumamoto University |
Principal Investigator |
Suzu Shinya 熊本大学, ヒトレトロウイルス学共同研究センター, 教授 (80363513)
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Co-Investigator(Kenkyū-buntansha) |
野依 修 熊本大学, ヒトレトロウイルス学共同研究センター, 特定事業研究員 (30737151)
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Project Period (FY) |
2017-04-01 – 2020-03-31
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Project Status |
Completed (Fiscal Year 2019)
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Budget Amount *help |
¥16,770,000 (Direct Cost: ¥12,900,000、Indirect Cost: ¥3,870,000)
Fiscal Year 2019: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2017: ¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
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Keywords | エイズ / 潜伏感染 / HIV-1 / fibrocytes / HIV / HIV潜伏感染 / Fibrocytes |
Outline of Final Research Achievements |
In this study, we identified fibrocytes as a candidate for HIV-1 latently infected cells. First, we revealed that fibrocytes are infected with HIV-1 through analyses of treatment-naïve patients, and mechanisms by which HIV-1 efficiently infects fibrocytes. We also found that the number of fibrocytes increases in HIV-1 infection, which persists even after long-term anti-retroviral therapy. Similar results were observed in monkeys infected with HIV-1-related monkey-tropic virus SIV. Finally, we revealed that not only resting CD4+ T cells but also fibrocytes are important HIV-1 latently infected cells through analyses of long-term treated patients whose viral load in plasma is undetectable.
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Academic Significance and Societal Importance of the Research Achievements |
潜伏感染は薬剤耐性ウイルスと並んで、エイズ研究領域で解決すべき重要な課題でとなっている。これまで代表的な潜伏感染細胞として静止期CD4+ T細胞が良く知られているが、排除する治療法は未だなく、そもそもこれらが潜伏感染全体をカバーするかもまだ明らかではない。従って、全ての潜伏感染細胞を一つずつ同定して、そしてそれらの相対的な貢献度を明確にする必要があり、本研究では私達のオリジナルのfibrocytesについて実践したものである。
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Report
(4 results)
Research Products
(15 results)
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[Journal Article] MPL activation directly induces fibrocyte differentiation to cause myelofibrosis2017
Author(s)
Maekawa T, Osawa Y, Izumi T, Nagao S, Takano K, Okada Y, Tachi N, Teramoto M, Kawamura T, Horiuchi T, Saga R, Kato S, Yamamura T, Watanabe J, Kobayashi A, Kobayashi S, Sato K, Hashimoto M, Suzu S, Kimura F
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Journal Title
Leukemia
Volume: 印刷中
Issue: 12
Pages: 2709-2716
DOI
Related Report
Peer Reviewed
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