Offer insight the mechanism of hepatitis B virus elimination by a novel regulated cell death type: ferroptosis.

深入了解一种新型调节细胞死亡类型：铁死亡，消除乙型肝炎病毒的机制。

• 批准号: 22K16033
• 负责人: 闕 路晟
• 金额: $ 3万
• 依托单位: National Institute of Infectious Diseases
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Early-Career Scientists
• 财政年份: 2022
• 资助国家: 日本
• 起止时间: 2022-04-01 至 2025-03-31
• 项目状态: 未结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-22K16033/
• 关键词: HBV; Ferroptosis; infected; clearance; ferroptosis

The Hepatitis B virus is a causative agent of Chronic hepatitis B, liver cirrhosis, and hepatocellular carcinoma. Current antiviral drugs interfering viral life cycle, have failed to eradicate infected cells, and the strategies to selectively eliminate infected cells have been awaited. Focusing on a novel type of cell death, the mechanism of how HBV and host immune response sensitize the infected cells to ferroptosis will be investigated.This year, we found a couple of anti/pro-ferroptotic genes expression is differentially expressed between no-HBV&HBV&HBV+anti-viral drug-treated in a dry/wet analysis; When a human hepatocyte cell line HepG2-NTCP was infected with HBV, a ferroptosis agonist and antagonist decreased and increased HBV infection by in-vitro experiment, respectively;

B型肝炎病毒是慢性B型肝炎、肝硬化和肝细胞癌的病原体。目前干扰病毒生命周期的抗病毒药物未能根除受感染的细胞，并且一直在等待选择性消除受感染细胞的策略。本研究的目的是探讨HBV和宿主免疫反应如何使感染细胞对铁凋亡敏感的机制，本研究在干/湿分析中发现了一对抗/促铁凋亡基因在无HBV和HBV及HBV+抗病毒药物处理的细胞中的差异表达;在体外实验中，当HBV感染人肝细胞系HepG 2-NTCP时，铁凋亡激动剂和拮抗剂分别降低和增加HBV感染;

项目成果

APOBEC3s mediated Merkel Cell Polyomavirus genome mutagenesis in the development of Merkel Cell Carcinoma

APOBEC3s 介导的默克尔细胞多瘤病毒基因组突变在默克尔细胞癌的发展中

• 发表时间: 2022
• 作者: 闕路晟;李瑩芳;大日輝記;柊元巌;西山智明;若江亨祥;村松正道
• 通讯作者: 村松正道

The role of APOBEC3s in Merkel Cell Polyomavirus evolution and Merkel Cell Carcinoma development

APOBEC3 在默克尔细胞多瘤病毒进化和默克尔细胞癌发展中的作用

• 发表时间: 2022
• 作者: Que L;Li Y;Dainichi T;Kukimoto I;Nishiyama T;Wakae K;Muramatsu M.
• 通讯作者: Muramatsu M.