Analysis of inflammatory mechanisms associated with HIV
| Project/Area Number |
17K15705
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Virology
|
|---|
| Research Institution | The University of Tokyo |
|---|
Principal Investigator |
Ishizaka Aya 東京大学, 医科学研究所, 特任研究員 (70746859)
|
|---|
| Project Period (FY) |
2017-04-01 – 2019-03-31
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
|---|
| Keywords | HIV / 潜伏感染 / 慢性炎症 / 免疫活性化 / ウィルス |
|---|
| Outline of Final Research Achievements |
In our previous study, we identified that short intracellular HIV-1 RNA (short transcripts, STs) is a biomarker of residual immune activation. In this study, we investigated which CD4+ T cell subsets are responsible for the expression of STs. We examined various CD4+ T cell subsets in peripheral blood from five patients who are STs-positive despite of suppressive antiretroviral therapy (ART) for two years. The main subsets which contribute to the expression of STs were central memory, early-differentiated and intermediate-differentiated effector memory CD4+ T cells.
|
| Academic Significance and Societal Importance of the Research Achievements |
現在の抗HIV療法ではHIV感染症は根治せず、患者体内では慢性的に炎症状態が続いている。我々のこれまでの解析から、HIV由来の短鎖RNAと慢性的な免疫の活性化との相関が明らかとなっている。本研究の成果と感染細胞内のプロウイルスの存在比を総合的に考察することで、ウイルスの転写の起きやすいサブセットの同定につながる。これらの解析から得られる知見は、残存感染細胞の持続的な転写活性化および慢性的な免疫賦活化が成立する分子基盤の理解に貢献する。
|
Report
(3 results)
Research Products
(1 results)
