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2018 Fiscal Year Final Research Report

Analysis of inflammatory mechanisms associated with HIV

Research Project

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Project/Area Number 17K15705
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Virology
Research InstitutionThe 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
KeywordsHIV / 潜伏感染 / 慢性炎症
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.

Free Research Field

ウイルス学

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。

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Published: 2020-03-30  

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