Hepatocyte-Specific Expression of the Hepatitis B Virus Core Promoter Depends on Both Positive and Negative Regulation

Guo, Weiwen; Chen, M; Yen, T. S. Benedict; Ou, Jing-Hsiung

doi:10.1128/mcb.13.1.443-448.1993

Cited by 45 publications

(1 citation statement)

References 20 publications

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“…On the other hand, this element regulates the basal core proteins (BCP) region in a position and orientation-dependent manner, functioning as a core upstream regulatory sequence, which overlaps the sequence of Enh-II [ 9 ]. Hepatocyte-enriched transcription factors, such as hepatocyte nuclear factor1 (HNF1) [ 10 ], HNF3 [ 11 , 12 ], HNF4 [ 13 , 14 ], CCAAT/enhancer-binding protein (C/EBP) [ 15 – 17 ], and fetoprotein transcription factor (FTF) [ 18 ], which are known to be responsible for the hepatocyte-specific Enh-II activity, and regulate its function [ 19 ]. Different mutations in the Enh-II region (as T1653 mutations in box-α) have been identified which are responsible for the development of HCC.…”

Section: Introductionmentioning

confidence: 99%

Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases

Khan

Gondal³

et al. 2022

PLoS ONE

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Background Hepatitis B Virus (HBV) is one of the most common human infectious agents, and the mutations in its genome may cause chronic hepatitis (CH), liver cirrhosis (LC), and hepatocellular carcinoma (HCC). This study was designed to characterize the enhancer-II (Enh-II) region of X gene in HBV positive patients to assess the association of such mutations with CH, LC, and HCC. Methods HBV positive samples (N = 200) with patients’ demographic and clinical data were collected from different regions of Khyber Pakhtunkhwa (KP), Pakistan. The Enh-II region of the HBx gene was sequenced and zanalyzed for polymorphism associated with advanced liver disease. Univariate and logistic regression analyses were performed to evaluate potent mutations associated with a risk for LC and HCC. Results HBV Enh-II region sequences analysis revealed 25 different mutations. The highest frequency of mutations S101F (62.2%), A102V/R/G/I (56.25%), M103L/A (68.75%)were found in HCC, followed in LC and CH patients as 57.1%, 42.8%, 28.52% 16%, 15.2% and 18.4% respectively. H94 deletion in the α-box of the Enh-II region, associated with a high risk of HCC was found in half of the HCC patients. This deletion was present in 28.5% of LC and 6.5% of CH patients. Importantly, the high frequency of some notable mutations such as E109A/Y, A110S/K, Y111D/E, and F112L was first time reported in the entire study population. The frequencies of these mutations were high in HCC (43.75%, 37.5%, 50% and 43.75% respectively) as compared to LC (14.28%, 14.28%, 28.2% and 42.8%) and CH patients (12.8%, 15.2%, 16.8% and 16% respectively). Conclusion Mutations associated with LC and HCC are prevalent in the Enh-II region in Pakistani HBV isolates. The mutations found are alarming in CH patients as these may progress to LC and HCC in a large number of patients.

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Section: Introductionmentioning

confidence: 99%

Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases

Khan

Gondal³

et al. 2022

PLoS ONE

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Hepatitis B Virus Genomes of Patients With Fulminant Hepatitis Do Not Share A Specific Mutation

et al. 1996

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The pathogenesis of fulminant hepatitis B virus (HBV) infection is not well understood. The aim of this study was to investigate whether there is an association between specific viral variants and a fulminant disease course. The entire HBV genomes from the serum of eight patients with fulminant HBV infection and one patient with fulminant hepatitis during reinfection after liver transplantation were investigated. After isolation and amplification of viral DNA by polymerase chain reaction (PCR), plus and minus strands were directly sequenced. Sequence data were analyzed by comparative sequence alignments with 35 and 2 complete HBV genome sequences from patients without and with fulminant hepatitis, respectively. Several point mutations were present in all regions of the genomes. Many nucleotide changes had never or rarely been found in the reported HBV isolates from patients without fulminant hepatitis. A distinct mutation present in all genomes was not identified. Clusters of rare and unique mutations were observed in the enhancer II core promoter region. Mutations previously suggested to be associated with fulminant HBV infection were not consistently found. A precore stop codon mutation at nucleotide position 1896 or an A-to-T mutation at nucleotide position 1762 and a G-to-A mutation at nucleotide position 1764 in the core promoter region were present in four and three cases, respectively. Fulminant HBV infection does not appear to be caused by a specific genomic mutation. However, various mutations clustering in the enhancer II core promoter region may contribute to a fulminant disease course.

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Lentiviral-Encoded Sodium Iodide Symporter-Mediated Cancer Gene Therapy

Ke¹,

Liu

2014

Gene Therapy of Cancer

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Hepatocyte-Specific Expression of the Hepatitis B Virus Core Promoter Depends on Both Positive and Negative Regulation

Cited by 45 publications

References 20 publications

Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases

Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases

Hepatitis B Virus Genomes of Patients With Fulminant Hepatitis Do Not Share A Specific Mutation

Lentiviral-Encoded Sodium Iodide Symporter-Mediated Cancer Gene Therapy

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