| Project/Area Number |
15K19588
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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 |
Infectious disease medicine
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| Research Institution | Kumamoto University |
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Principal Investigator |
MURAKOSHI HAYATO 熊本大学, エイズ学研究センター, 特任講師 (60646123)
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| Research Collaborator |
GATANAGA Hiroyuki
CHIKATA Takayuki
AKAHOSHI Tomohiro
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 細胞傷害性T細胞 / HIV / HLA |
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| Outline of Final Research Achievements |
To clarify this mechanism, we identified HLA-B*35:01-restricted epitope-specific CD8+ T cells controlling HIV-1 in 63 HIV-1 clade B-infected Japanese individuals having HLA-B*35:01 and further analyzed the effect of mutations within the epitopes on the T cell responses. The T cell responses to GagNY9, PolVY10, NefRY11, or YF9 epitopes were significantly associated with low plasma viral load. A breadth of the T cell responses to these 4 epitopes was inversely correlated with it. The control of HIV-1 by YF9-specific T cells are impaired by NefY135F mutation associated with HLA-A*24:02. The ex vivo longitudinal analysis of the YF9-specific T cells showed that the Y135F mutant-specific T cells and wild type-specific/cross-reactive T cells were elicited before and after an emergence of the mutant virus. However, the former T cells failed to control HIV-1 replication whereas the latter T cells contributed to the control of HIV-1.
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