scholarly journals Different hepatitis b virus genotypes are associated with different mutations in the core promoter and precore regions during hepatitis B e antigen seroconversion

Hepatology ◽  
1999 ◽  
Vol 29 (3) ◽  
pp. 976-984 ◽  
Author(s):  
Henry L. Y. Chan ◽  
Munira Hussain ◽  
Anna S. F. Lok
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Core Promoter ◽  
Hepatitis B E Antigen ◽  
The Core ◽  
B Virus ◽  
Virus Genotypes

scholarly journals High Frequency of Either Altered Pre-Core Start Codon or Weakened Kozak Sequence in the Core Promoter Region in Hepatitis B Virus A1 Strains from Rwanda

Genes ◽  
2019 ◽  
Vol 10 (3) ◽  
pp. 182 ◽  
Author(s):  
Heléne Norder ◽  
Theogene Twagirumugabe ◽  
Joanna Said ◽  
Yarong Tian ◽  
Ka-Wei Tang ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Promoter Region ◽  
Core Promoter ◽  
Etiologic Agent ◽  
Start Codon ◽  
Core Promoter Region ◽  
Kozak Sequence ◽  
The Core ◽  
B Virus

Hepatitis B virus (HBV) is endemic in Rwanda and is a major etiologic agent for chronic liver disease in the country. In a previous analysis of HBV strains from Rwanda, the S genes of most strains segregated into one single clade of subgenotype, A1. More than half (55%) of the anti-HBe positive individuals were viremic. In this study, 23 complete HBV genomes and the core promoter region (CP) from 18 additional strains were sequenced. Phylogenetic analysis of complete genomes confirmed that most Rwandan strain formed a single unique clade, within subgenotype A1. Strains from 17 of 22 (77%) anti-HBe positive HBV carriers had either mutated the precore start codon (9 strains with either CUG, ACG, UUG, or AAG) or mutations in the Kozak sequence preceding the pre-core start codon (8 strains). These mutually exclusive mutations were also identified in subgenotypes A1 (70/266; 26%), A2 (12/255; 5%), and A3 (26/49; 53%) sequences from the GenBank. The results showed that previous, rarely described HBV variants, expressing little or no HBeAg, are selected in anti-HBe positive subgenotype Al carriers from Rwanda and that mutations reducing HBeAg synthesis might be unique for a particular HBV clade, not just for a specific genotype or subgenotype.

Mutations in the core promoter region of hepatitis B virus in patients with chronic hepatitis B

1996 ◽  
Vol 49 (2) ◽  
pp. 115-123 ◽  
Author(s):  
Masayuki Kurosaki ◽  
Nobuyuki Enomoto ◽  
Yasuhiro Asahina ◽  
Ikuo Sakuma ◽  
Takaaki Ikeda ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Chronic Hepatitis B ◽  
Promoter Region ◽  
Core Promoter ◽  
Core Promoter Region ◽  
The Core ◽  
B Virus

Characterization of the core promoter and enhancer of duck hepatitis B virus

Virology ◽  
1991 ◽  
Vol 184 (1) ◽  
pp. 242-252 ◽  
Author(s):  
Chen Liu ◽  
Lynn D. Condreay ◽  
John B.E. Burch ◽  
William Mason
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Core Promoter ◽  
Duck Hepatitis B Virus ◽  
The Core ◽  
Duck Hepatitis ◽  
B Virus

scholarly journals Hepatocyte-specific expression of the hepatitis B virus core promoter depends on both positive and negative regulation.

1993 ◽  
Vol 13 (1) ◽  
pp. 443-448 ◽  
Author(s):  
W Guo ◽  
M Chen ◽  
T S Yen ◽  
J H Ou
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Mammalian Cells ◽  
Core Promoter ◽  
Regulatory Sequence ◽  
Cell Type Specificity ◽  
Specific Expression ◽  
The Core ◽  
Upstream Regulatory Sequence ◽  
B Virus

The core promoter of hepatitis B virus shows hepatocyte specificity, which is largely dependent on an upstream regulatory sequence that overlaps with viral enhancer II. Footprint analyses by numerous groups have shown binding by cellular proteins over a large stretch of DNA in this region, but the identity of these proteins and their role in core promoter function remain largely unknown. We present data showing that the transcription factor HNF-4 is one such factor, as it activates the core promoter approximately 20-fold via a binding site within the upstream regulatory sequence. Since HNF-4 is enriched in hepatocytes, its involvement at least partially explains the hepatocyte specificity of this promoter. In addition, however, we have found a region upstream of the HNF-4 site that suppresses activation by HNF-4 in HeLa cells but not in hepatoma cells. Therefore, the cell type specificity of the core promoter appears to result from a combination of activation by one or more factors specifically enriched in hepatocytes and repression by some other factor(s) present in nonhepatocytes, and it may provide a convenient model system for studying this type of tissue-specific transcriptional regulation in mammalian cells.

scholarly journals Regulation of Hepatitis B Virus Core Promoter by Transcription Factors HNF1 and HNF4 and the Viral X Protein

2004 ◽  
Vol 78 (13) ◽  
pp. 6908-6914 ◽  
Author(s):  
Yanyan Zheng ◽  
Jie Li ◽  
Jing-hsiung Ou
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Binding Site ◽  
Nuclear Receptors ◽  
Double Mutant ◽  
Core Promoter ◽  
X Protein ◽  
Double Mutation ◽  
The Core ◽  
B Virus

ABSTRACT Hepatitis B virus (HBV) core promoter contains a binding site for nuclear receptors. A natural double mutation in this binding site, which changes nucleotide (nt) 1765 from A to T and nt 1767 from G to A, selectively abolishes the binding of several nuclear receptors without affecting that of HNF4. This double mutation also creates a binding site for the transcription factor HNF1 and changes two amino acids in the overlapping X protein sequence. In this study, we have examined the roles of HNF1, HNF4, and the X protein in the regulation of the core promoter activities in Huh7 hepatoma cells. Our results indicate that HNF4 could stimulate the expression of the precore RNA and the core RNA from the core promoter of both the wild-type (WT) HBV and the double mutant, although its effect on the former was more prominent. In contrast, HNF1, which did not affect the WT core promoter, suppressed the precore RNA expression of the double mutant. Further analysis using HBV genomic constructs, with and without the ability to express the X protein, indicates that the X protein did not affect the HNF4 activity on the core promoter and affected the HNF1 activity on the core promoter of only the double mutant. Thus, our results indicate that the phenotypic differences of HBV WT and double-mutant core promoters are at least partially due to the differential activities of HNF1, HNF4, and the X protein on these two promoters.

Naturally occurring hepatitis B virus mutants with deletions in the core promoter region

1994 ◽  
Vol 20 (6) ◽  
pp. 837-841 ◽  
Author(s):  
Tomasz Laskus ◽  
Jorge Rakela ◽  
Myron J. Tong ◽  
Marek J. Nowicki ◽  
James W. Mosley ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Promoter Region ◽  
Core Promoter ◽  
Core Promoter Region ◽  
The Core ◽  
Naturally Occurring ◽  
B Virus

T1762A1764 core promoter mutation in hepatitis B virus genome and hepatitis B e antigen seroconversion in school-aged young carriers

2000 ◽  
Vol 118 (4) ◽  
pp. A935
Author(s):  
Ryo Fukuda ◽  
Mohammad Ak Rumi ◽  
Sachiko Hamamoto ◽  
Norihisa Ishimura ◽  
Shunji Ishihara ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Core Promoter ◽  
Virus Genome ◽  
Promoter Mutation ◽  
Hepatitis B E Antigen ◽  
B Virus ◽  
Core Promoter Mutation
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