2021 Fiscal Year Final Research Report
Influences of the HTLV-1 viral activities in the determination of the infected cell-fate via hijacking the micro-environment of infected cells
Project/Area Number |
19K07573
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 49060:Virology-related
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Research Institution | The University of Tokyo |
Principal Investigator |
Kazumi Nakano 東京大学, 大学院新領域創成科学研究科, 准教授 (60549591)
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Project Period (FY) |
2019-04-01 – 2022-03-31
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Keywords | HTLV-1 / Rex / Tax / Hbz / 潜伏感染細胞 / ウイルス発がん / 感染細胞微小環境 / T細胞 |
Outline of Final Research Achievements |
HTLV-1 is an oncovirus that infects human T cells and causes ATL after several decades. However, only about 5% of carriers develop ATL, and many infected cells remain disease-free latently infected cells for several decades. We aimed to elucidate the mechanism of the establishment of such infected cells. In particular, we focused on the role of Rex, which is one of the most unknown viral proteins. We found that Rex affects gene expression regulation, immune responses, and signaling pathways through interactions with various proteins in addition to its function in viral mRNA transport, and that HTLV-1-infected cells are formed through the interaction of Rex, Tax, Hbz, and other viral proteins.
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Free Research Field |
ウイルス腫瘍学
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Academic Significance and Societal Importance of the Research Achievements |
ATLは感染細胞の腫瘍化により発症する。しかしほとんどのキャリア体内でHTLV-1感染細胞はdisease-freeな潜伏感染状態を維持する。よってATLは本来のウイルスのプログラムを逸脱した状態と言える。本研究ではHTLV-1感染実験系やRex、Tax、Hbzの単独または共発現系を駆使し、現実的なHTLV-1感染の場での解析を目指した。その結果1ウイルスタンパク質群の働きによる感染細胞の構築メカニズムの一端が明らかにした。このようにHTLV-1の本来のdisease-freeな潜伏感染細胞構築メカニズムを解明することにより、感染細胞の腫瘍化(ATL発症)メカニズムの理解が深まると期待される。
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