Human BST-2/tetherin inhibits Junin virus release from host cells and its inhibition is partially counteracted by viral nucleoprotein

• Material Type: 博士論文
• Title: Human BST-2/tetherin inhibits Junin virus release from host cells and its inhibition is partially counteracted by viral nucleoprotein
• Author/Editor: Rajabali, Zadeh Vahid
• Author Heading: Rajabali, Zadeh Vahid
• Publication, Distribution, etc.: Microbiology Society
• Publication Date: 2020-09-18
• Publication Date (W3CDTF): 2020-09-18
• Alternative Title: ヒトBST-2/tetherinはフニンウイルスの宿主細胞からの放出を阻害し、その阻害作用はウイルス核タンパク質により部分的に相殺される。
• Periodical title: Journal of General Virology
• No. or year of volume/issue: 101 6
• Volume: 101
• Issue: 6
• Pages: 573-586
• ISSN (Periodical Title): ISSN : 0022-1317; ISSN : 1465-2099
• Degree grantor/type: Nagasaki University (長崎大学)
• Date Granted: 2020-09-18
• Dissertation Number: 甲医歯薬第1266号
• Degree Type: 博士(医学)
• Text Language Code: eng
• Subject Heading: Junin virus; Arenaviridae; human BST-2; innate immunity; Tetherin
• Target Audience: 一般
• Note (General): Bone marrow stromal cell antigen-2 (BST-2), also known as tetherin, is an interferon-inducible membrane-associated protein. It effectively targets enveloped viruses at the release step of progeny viruses from host cells, thereby restricting the further spread of viral infection. Junin virus (JUNV) is a member of Arenaviridae, which causes Argentine haemorrhagic fever that is associated with a high rate of mortality. In this study, we examined the effect of human BST-2 on the replication and propagation of JUNV. The production of JUNV Z-mediated virus-like particles (VLPs) was significantly inhibited by over-expression of BST-2. Electron microscopy analysis revealed that BST-2 functions by forming a physical link that directly retains VLPs on the cell surface. Infection using JUNV showed that infectious JUNV production was moderately inhibited by endogenous or exogenous BST-2. We also observed that JUNV infection triggers an intense interferon response, causing an upregulation of BST-2, in infected cells. However, the expression of cell surface BST-2 was reduced upon infection. Furthermore, the expression of JUNV nucleoprotein (NP) partially recovered VLP production from BST-2 restriction, suggesting that the NP functions as an antagonist against antiviral effect of BST-2. We further showed that JUNV NP also rescued the production of Ebola virus VP40-mediated VLP from BST-2 restriction as a broad spectrum BST-2 antagonist. To our knowledge, this is the first report showing that an arenavirus protein counteracts the antiviral function of BST-2.; 長崎大学学位論文 学位記番号:博(医歯薬)甲第1266号 学位授与年月日:令和2年9月18日; Author: Vahid Rajabali Zadeh?, Shuzo Urata?, Miako Sakaguchi, Jiro Yasuda?; Citation: Journal of General Virology, 101(6), pp.573-586; 2020; identifier:Nagasaki University (長崎大学), 博士(医学) (2020-09-18)
• Source: fulltext; https://nagasaki-u.repo.nii.ac.jp/?action=repository_action_common_download&item_id=47&item_no=1&attribute_id=70&file_no=1
• Access Restrictions: インターネット公開
• Rights (production): c 2020 The Authors. The definitive peer reviewed, edited version of this article is published in Journal of General Virology, 101(6), 2020, https://doi.org/10.1099/jgv.0.001414.
• Related Material: http://hdl.handle.net/10069/40270
• Related Material (DOI): 10.1099/jgv.0.001414
• Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）; https://irdb.nii.ac.jp
• Original Data Provider (Database): 長崎大学 : 長崎大学学術研究成果リポジトリ