Role of A3G acetylation and Vif/HDAC3 complex in HIV-1 infection

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K08809
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Virology
• Research Institution: Kyoto University
• Principal Investigator: Shirakawa Kotaro 京都大学, 医学研究科, 助教 (80728270)
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: HIV-1 / Vif / ヒストン脱アセチル化酵素 / DNAシトシン脱アミノ化酵素APOBEC3G / 潜伏感染

Outline of Final Research Achievements

1) We identified that five lysine residues of APOBEC3G are aceylated and deacetylated by HDAC3. Its non-acetylated Arginine mutant is less sensitive to Vif mediated degradation.
2) Latently HIV-1 infected T-cells are sorted and its gene expression profile is compared to virus producing cells and non-infected cells. We identified 33 genes specifically down-regulated in latently infected cells and two genes specifically up-regulated genes compared to non-infected cells.

Free Research Field

ウイルス学

Academic Significance and Societal Importance of the Research Achievements

ウイルスが細胞のメカニズムをハイジャックして利用するその一端を発見した。HIV-1感染症を克服するためには、潜伏感染するために必要なメカニズムを明らかにする必要があり、本研究で潜伏感染細胞を分離しその遺伝子発現変化を解析できたことは新たなステップになると考えられる。