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

Szczegóły
Abstrakt

Tytuł:: Hepatitis B virus rigs the cellular metabolome to avoid innate immune recognition.
Autorzy:: Zhou L; State Key Laboratory of Virology, Modern Virology Research Center, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
He R; State Key Laboratory of Virology, Modern Virology Research Center, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Fang P; State Key Laboratory of Virology, Modern Virology Research Center, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Li M; State Key Laboratory of Virology, Modern Virology Research Center, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Yu H; State Key Laboratory of Virology, Modern Virology Research Center, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Wang Q; College of Bioscience and Biotechnology, Hunan Agricultural University, Changsha, 410128, China.
Yu Y; The Key Laboratory of Biosystems Homeostasis and Protection of the Ministry of Education and Innovation Center for Cell Signaling Network, Life Sciences Institute, Zhejiang University, Hangzhou, China.
Wang F; Department of Laboratory Medicine, Zhongnan Hospital of Wuhan University, Wuhan, China.
Zhang Y; Hubei Provincial Cooperative Innovation Center of Industrial Fermentation, College of Food and Pharmaceutical Engineering, Hubei University of Technology, Wuhan, 430068, China.
Chen A; Department of Physiology, Nanjing Medical University, Nanjing, 211166, China.
Peng N; State Key Laboratory of Virology, Modern Virology Research Center, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Lin Y; The Key Laboratory of Molecular Biology of Infectious Diseases designated by the Chinese Ministry of Education, Chongqing Medical University, Chongqing, China.
Zhang R; Department of Hepato-Pancreato-Biliary Surgery, SunYat-sen Memorial Hospital, SunYat-sen University, Guangzhou, 510120, China.
Trilling M; Institute for Virology, University Hospital Essen, University of Duisburg-Essen, Essen, 45122, Germany.
Broering R; Department of Gastroenterology and Hepatology, University Hospital Essen, University of Duisburg-Essen, Essen, 45122, Germany.
Lu M; Institute for Virology, University Hospital Essen, University of Duisburg-Essen, Essen, 45122, Germany.
Zhu Y; State Key Laboratory of Virology, Modern Virology Research Center, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Liu S; State Key Laboratory of Virology, Modern Virology Research Center, College of Life Sciences, Wuhan University, Wuhan, 430072, China. liushi_.
Źródło:: Nature communications [Nat Commun] 2021 Jan 04; Vol. 12 (1), pp. 98. Date of Electronic Publication: 2021 Jan 04.
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Original Publication: [London] : Nature Pub. Group
MeSH Terms:: Immunity, Innate*
Metabolome*
Hepatitis B virus/*physiology
Adaptor Proteins, Signal Transducing/metabolism ; Anaerobiosis ; Animals ; Cells, Cultured ; DEAD Box Protein 58/metabolism ; Glucose/metabolism ; Glycolysis ; Hep G2 Cells ; Hepatocytes/metabolism ; Hepatocytes/pathology ; Hepatocytes/virology ; Humans ; Immune Evasion ; Interferons/metabolism ; Lactic Acid/metabolism ; Mice, Inbred C57BL ; Models, Biological ; Signal Transduction ; Virion/metabolism ; Mice
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Substance Nomenclature:: 0 (Adaptor Proteins, Signal Transducing)
0 (MAVS protein, human)
33X04XA5AT (Lactic Acid)
9008-11-1 (Interferons)
EC 3.6.4.13 (DEAD Box Protein 58)
IY9XDZ35W2 (Glucose)
Entry Date(s):: Date Created: 20210105 Date Completed: 20210114 Latest Revision: 20240226
Update Code:: 20240226
PubMed Central ID:: PMC7782485
DOI:: 10.1038/s41467-020-20316-8
PMID:: 33397935
: Czasopismo naukowe

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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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