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甲型流感病毒基质蛋白2的质子通道活性导致自噬停滞。

Proton Channel Activity of Influenza A Virus Matrix Protein 2 Contributes to Autophagy Arrest.

作者信息

Ren Yizhong, Li Chufang, Feng Liqiang, Pan Weiqi, Li Liang, Wang Qian, Li Jiashun, Li Na, Han Ling, Zheng Xuehua, Niu Xuefeng, Sun Caijun, Chen Ling

机构信息

School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, China State Key Laboratory of Respiratory Disease Guangzhou Institutes of Biomedicine and Health, Guangzhou, Guangdong, China.

State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China

出版信息

J Virol. 2015 Oct 14;90(1):591-8. doi: 10.1128/JVI.00576-15. Print 2016 Jan 1.

Abstract

Influenza A virus infection can arrest autophagy, as evidenced by autophagosome accumulation in infected cells. Here, we report that this autophagosome accumulation can be inhibited by amantadine, an antiviral proton channel inhibitor, in amantadine-sensitive virus infected cells or cells expressing influenza A virus matrix protein 2 (M2). Thus, M2 proton channel activity plays a role in blocking the fusion of autophagosomes with lysosomes, which might be a key mechanism for arresting autophagy.

摘要

甲型流感病毒感染可抑制自噬,感染细胞中自噬体的积累即为证据。在此,我们报告,在对金刚烷胺敏感的病毒感染细胞或表达甲型流感病毒基质蛋白2(M2)的细胞中,这种自噬体积累可被抗病毒质子通道抑制剂金刚烷胺抑制。因此,M2质子通道活性在阻止自噬体与溶酶体融合中发挥作用,这可能是抑制自噬的关键机制。

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