Glutamate dehydrogenase 1-dependent α-ketoglutarate promotes hepatitis B virus transcription by modulating histone methylations on the covalently closed circular DNA minichromosome

Background/Aims Hepatitis B virus (HBV) hijacks host cell metabolism, especially host glutamine metabolism, to support its replication. Glutamate dehydrogenase 1 (GDH1), a mitochondrial enzyme crucial for glutamine metabolism, can interact with histone demethylases to regulate gene expression throug...

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Main Authors: Sheng-Tao Cheng, Wei-Xian Chen, Hai-Jun Deng, Xin He, Hui Zhang, Ming Tan, Hai-Bo Yu, Zhen-Zhen Zhang, Ji-Hua Ren, Min-Li Yang, Da-Peng Zhang, Zhi-Hong Li, Juan Chen
Format: Article
Language:English
Published: Korean Association for the Study of the Liver 2025-07-01
Series:Clinical and Molecular Hepatology
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Online Access:http://e-cmh.org/upload/pdf/cmh-2024-0694.pdf
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author Sheng-Tao Cheng
Wei-Xian Chen
Hai-Jun Deng
Xin He
Hui Zhang
Ming Tan
Hai-Bo Yu
Zhen-Zhen Zhang
Ji-Hua Ren
Min-Li Yang
Da-Peng Zhang
Zhi-Hong Li
Juan Chen
author_facet Sheng-Tao Cheng
Wei-Xian Chen
Hai-Jun Deng
Xin He
Hui Zhang
Ming Tan
Hai-Bo Yu
Zhen-Zhen Zhang
Ji-Hua Ren
Min-Li Yang
Da-Peng Zhang
Zhi-Hong Li
Juan Chen
author_sort Sheng-Tao Cheng
collection DOAJ
description Background/Aims Hepatitis B virus (HBV) hijacks host cell metabolism, especially host glutamine metabolism, to support its replication. Glutamate dehydrogenase 1 (GDH1), a mitochondrial enzyme crucial for glutamine metabolism, can interact with histone demethylases to regulate gene expression through histone methylation. However, the mechanisms underlying GDH1-mediated glutamine metabolism reprogramming and the roles of key metabolites during HBV infection remain unclear. Methods Transcriptomic and metabolomic analyses of HBV-infected cell were performed. Both HBV-infected cells and humanized liver chimeric mice were used to elucidate the effect of glutamine metabolism on HBV. Results HBV infection leads to the abnormal activation of glutamine metabolism, including upregulation of key enzymes and metabolites involved in glutamine metabolism. The viral core protein (HBc) mediates the translocation of GDH1 into the nucleus, where GDH1 activates covalently closed circular DNA (cccDNA) transcription by converting glutamate to α-ketoglutarate (αKG). Mechanistically, the promoting effect of GDH1-derived αKG on cccDNA transcription is independent of its conventional role. Rather, αKG directly interacts with the lysine-specific demethylase KDM4A and enhances KDM4A demethylase activity to regulate αKG-dependent histone demethylation, controlling cccDNA transcription. Conclusions Our findings highlight the importance of glutamine metabolism in HBV transcription and suggest that glutamine deprivation is a potential strategy for silencing cccDNA transcription.
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issn 2287-2728
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language English
publishDate 2025-07-01
publisher Korean Association for the Study of the Liver
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spelling doaj-art-1660af7e6fc547f0bcadd2a65fbba69c2025-08-20T03:17:26ZengKorean Association for the Study of the LiverClinical and Molecular Hepatology2287-27282287-285X2025-07-0131384186510.3350/cmh.2024.06942159Glutamate dehydrogenase 1-dependent α-ketoglutarate promotes hepatitis B virus transcription by modulating histone methylations on the covalently closed circular DNA minichromosomeSheng-Tao Cheng0Wei-Xian Chen1Hai-Jun Deng2Xin He3Hui Zhang4Ming Tan5Hai-Bo Yu6Zhen-Zhen Zhang7Ji-Hua Ren8Min-Li Yang9Da-Peng Zhang10Zhi-Hong Li11Juan Chen12 Department of Clinical Laboratory, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China Department of Clinical Laboratory, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China The Key Laboratory of Molecular Biology of Infectious Diseases designated by the Chinese Ministry of Education, Chongqing Medical University, Chongqing, China State Key Laboratory of Ultrasound in Medicine and Engineering, College of Biomedical Engineering, Chongqing Medical University, Chongqing, China The Key Laboratory of Molecular Biology of Infectious Diseases designated by the Chinese Ministry of Education, Chongqing Medical University, Chongqing, China The Key Laboratory of Molecular Biology of Infectious Diseases designated by the Chinese Ministry of Education, Chongqing Medical University, Chongqing, China The Key Laboratory of Molecular Biology of Infectious Diseases designated by the Chinese Ministry of Education, Chongqing Medical University, Chongqing, China Department of Infectious Disease, Children’s Hospital of Chongqing Medical University, Chongqing, China The Key Laboratory of Molecular Biology of Infectious Diseases designated by the Chinese Ministry of Education, Chongqing Medical University, Chongqing, China The Key Laboratory of Molecular Biology of Infectious Diseases designated by the Chinese Ministry of Education, Chongqing Medical University, Chongqing, China The Key Laboratory of Molecular Biology of Infectious Diseases designated by the Chinese Ministry of Education, Chongqing Medical University, Chongqing, China The Key Laboratory of Molecular Biology of Infectious Diseases designated by the Chinese Ministry of Education, Chongqing Medical University, Chongqing, China Department of Clinical Laboratory, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaBackground/Aims Hepatitis B virus (HBV) hijacks host cell metabolism, especially host glutamine metabolism, to support its replication. Glutamate dehydrogenase 1 (GDH1), a mitochondrial enzyme crucial for glutamine metabolism, can interact with histone demethylases to regulate gene expression through histone methylation. However, the mechanisms underlying GDH1-mediated glutamine metabolism reprogramming and the roles of key metabolites during HBV infection remain unclear. Methods Transcriptomic and metabolomic analyses of HBV-infected cell were performed. Both HBV-infected cells and humanized liver chimeric mice were used to elucidate the effect of glutamine metabolism on HBV. Results HBV infection leads to the abnormal activation of glutamine metabolism, including upregulation of key enzymes and metabolites involved in glutamine metabolism. The viral core protein (HBc) mediates the translocation of GDH1 into the nucleus, where GDH1 activates covalently closed circular DNA (cccDNA) transcription by converting glutamate to α-ketoglutarate (αKG). Mechanistically, the promoting effect of GDH1-derived αKG on cccDNA transcription is independent of its conventional role. Rather, αKG directly interacts with the lysine-specific demethylase KDM4A and enhances KDM4A demethylase activity to regulate αKG-dependent histone demethylation, controlling cccDNA transcription. Conclusions Our findings highlight the importance of glutamine metabolism in HBV transcription and suggest that glutamine deprivation is a potential strategy for silencing cccDNA transcription.http://e-cmh.org/upload/pdf/cmh-2024-0694.pdfglutaminegdh1αkgcccdnamethylation
spellingShingle Sheng-Tao Cheng
Wei-Xian Chen
Hai-Jun Deng
Xin He
Hui Zhang
Ming Tan
Hai-Bo Yu
Zhen-Zhen Zhang
Ji-Hua Ren
Min-Li Yang
Da-Peng Zhang
Zhi-Hong Li
Juan Chen
Glutamate dehydrogenase 1-dependent α-ketoglutarate promotes hepatitis B virus transcription by modulating histone methylations on the covalently closed circular DNA minichromosome
Clinical and Molecular Hepatology
glutamine
gdh1
αkg
cccdna
methylation
title Glutamate dehydrogenase 1-dependent α-ketoglutarate promotes hepatitis B virus transcription by modulating histone methylations on the covalently closed circular DNA minichromosome
title_full Glutamate dehydrogenase 1-dependent α-ketoglutarate promotes hepatitis B virus transcription by modulating histone methylations on the covalently closed circular DNA minichromosome
title_fullStr Glutamate dehydrogenase 1-dependent α-ketoglutarate promotes hepatitis B virus transcription by modulating histone methylations on the covalently closed circular DNA minichromosome
title_full_unstemmed Glutamate dehydrogenase 1-dependent α-ketoglutarate promotes hepatitis B virus transcription by modulating histone methylations on the covalently closed circular DNA minichromosome
title_short Glutamate dehydrogenase 1-dependent α-ketoglutarate promotes hepatitis B virus transcription by modulating histone methylations on the covalently closed circular DNA minichromosome
title_sort glutamate dehydrogenase 1 dependent α ketoglutarate promotes hepatitis b virus transcription by modulating histone methylations on the covalently closed circular dna minichromosome
topic glutamine
gdh1
αkg
cccdna
methylation
url http://e-cmh.org/upload/pdf/cmh-2024-0694.pdf
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