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PRKAA/AMPK restricts HBV replication through promotion of autophagic degradation.

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机构： [1]State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy , Chengdu , China. [2]Department of Neurology , the Affiliated Hospital of Hainan Medical College , Haikou , China. [3]Department of General Surgery , West China Hospital, Sichuan University , Chengdu , China. [4]Department of Biochemistry and Molecular Biology , and Molecular Medicine and Cancer Research Center, Chongqing Medical University , Chongqing , China. [5]Lab for Aging Research, Center for Medical Stem Cell Biology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University , Chengdu , China. [6]Center of Infectious Diseases, West China Hospital, Sichuan University , Chengdu , Sichuan , China. [7]School of Medicine, Nankai University , Tianjin , China. [8]Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong , Hong Kong , China. [9]Department of Molecular Microbiology and Immunology , Norris Comprehensive Cancer Center, University of Southern California , Los Angeles , CA , USA. [10]Department of Biochemistry and Molecular Biology , Monash University , Clayton , Victoria , Australia. [11]Department of Liver Surgery , West China Hospital, Sichuan University , Chengdu , China.

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Adenosine monophosphate-activated protein kinase (AMPK) is a crucial energy sensor that maintains cellular energy homeostasis. AMPK plays a critical role in macroautophagy/autophagy, and autophagy facilitates hepatitis B virus (HBV) replication. To date, the intrinsic link among AMPK, autophagy and HBV production remains to be elucidated. Here, we demonstrate that PRKAA (a catalytic subunit of AMPK) is activated in response to HBV-induced oxidative stress, which in turn decreases the production of HBV. Mechanistic studies reveal that the autophagy machinery is associated with the inhibitory effect of PRKAA/AMPK on HBV production. Activation of PRKAA/AMPK promotes autolysosome-dependent degradation through stimulation of cellular ATP levels, which then leads to the depletion of autophagic vacuoles. Taken together, our data suggest that the activation of AMPK might be a stress response of host cells to restrict virus production through promotion of autophagic degradation. These findings therefore indicate that AMPK could provide a potential therapeutic target for HBV infection.

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出版当年[2016]版：

大类 | 1 区

生物

小类 | 2 区细胞生物学

最新[2023]版：

大类 | 1 区

生物学

小类 | 2 区细胞生物学

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第一作者机构： [1]State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy , Chengdu , China.

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通讯机构： [1]State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy , Chengdu , China. [2]Department of Neurology , the Affiliated Hospital of Hainan Medical College , Haikou , China. [11]Department of Liver Surgery , West China Hospital, Sichuan University , Chengdu , China. [*1]State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy, Chengdu, 610041, China [*2]Department of Liver Surgery, West China Hospital, Sichuan University, Chengdu, 610041, China [*3]Department of Neurology, Affiliated Hospital of Hainan Medical College, Haikou, 570102, China.

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