PRKAA/AMPK restricts HBV replication through promotion of autophagic degradation
Na Xie
Kefei Yuan
Li Zhou
Kui Wang
Hai-Ning Chen
Yunlong Lei
Jiang Lan
Qinqin Pu
Wei Gao
Lu Zhang
Guobo Shen
Qifu Li
Hengyi Xiao
Hong Tang
Rong Xiang
Mingliang He
Pinghui Feng
Edouard C. Nice
Yuquan Wei
Haiyuan Zhang
Jiayin Yang
Canhua Huang
10.6084/m9.figshare.3439148.v1
https://tandf.figshare.com/articles/dataset/PRKAA_AMPK_restricts_HBV_replication_through_promotion_of_autophagic_degradation/3439148
<p>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.</p>
2016-06-16 14:58:05
adenosine monophosphate-activated protein kinase
adenosine triphosphate
autophagy
hepatitis B virus
oxidative stress