Hepatitis B virus rigs the cellular metabolome to avoid innate immune recognition

Li Zhou, Rui He, Peining Fang, Mengqi Li, Haisheng Yu, Qiming Wang, Yi Yu, Fubing Wang, Yi Zhang, Aidong Chen, Nanfang Peng, Yong Lin, Rui Zhang, Mirko Trilling, Ruth Broering, Mengji Lu, Ying Zhu and Shi Liu ()
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Li Zhou: College of Life Sciences, Wuhan University
Rui He: College of Life Sciences, Wuhan University
Peining Fang: College of Life Sciences, Wuhan University
Mengqi Li: College of Life Sciences, Wuhan University
Haisheng Yu: College of Life Sciences, Wuhan University
Qiming Wang: Hunan Agricultural University
Yi Yu: Zhejiang University
Fubing Wang: Zhongnan Hospital of Wuhan University
Yi Zhang: Hubei University of Technology
Aidong Chen: Nanjing Medical University
Nanfang Peng: College of Life Sciences, Wuhan University
Yong Lin: Chongqing Medical University
Rui Zhang: SunYat-sen Memorial Hospital, SunYat-sen University
Mirko Trilling: University Hospital Essen, University of Duisburg-Essen
Ruth Broering: University Hospital Essen, University of Duisburg-Essen
Mengji Lu: University Hospital Essen, University of Duisburg-Essen
Ying Zhu: College of Life Sciences, Wuhan University
Shi Liu: College of Life Sciences, Wuhan University

Nature Communications, 2021, vol. 12, issue 1, 1-13

Abstract: Abstract Glucose metabolism and innate immunity evolved side-by-side. It is unclear if and how the two systems interact with each other during hepatitis B virus (HBV) infections and, if so, which mechanisms are involved. Here, we report that HBV activates glycolysis to impede retinoic acid-inducible gene I (RIG-I)-induced interferon production. We demonstrate that HBV sequesters MAVS from RIG-I by forming a ternary complex including hexokinase (HK). Using a series of pharmacological and genetic approaches, we provide in vitro and in vivo evidence indicating that HBV suppresses RLR signaling via lactate dehydrogenase-A-dependent lactate production. Lactate directly binds MAVS preventing its aggregation and mitochondrial localization during HBV infection. Therefore, we show that HK2 and glycolysis-derived lactate have important functions in the immune escape of HBV and that energy metabolism regulates innate immunity during HBV infection.

Date: 2021
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DOI: 10.1038/s41467-020-20316-8

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