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

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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.

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Zhou, L., He, R., Fang, P., Li, M., Yu, H., Wang, Q., … Liu, S. (2021). Hepatitis B virus rigs the cellular metabolome to avoid innate immune recognition. Nature Communications, 12(1). https://doi.org/10.1038/s41467-020-20316-8

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