Mutations in the Core Promoter/Enhancer II Regions of Naturally Occurring Hepatitis B Virus Variants and Analysis of the Effects on Transcription Activities

Intervirology ◽  
1995 ◽  
Vol 38 (5) ◽  
pp. 290-294 ◽  
Author(s):  
Akira Nishizono ◽  
Masaharu Hiraga ◽  
Kazuhiro Kohno ◽  
Yoshiko T. Sonoda ◽  
Hideo Terao ◽  
...  
1994 ◽  
Vol 20 (6) ◽  
pp. 837-841 ◽  
Author(s):  
Tomasz Laskus ◽  
Jorge Rakela ◽  
Myron J. Tong ◽  
Marek J. Nowicki ◽  
James W. Mosley ◽  
...  

Virology ◽  
2007 ◽  
Vol 365 (2) ◽  
pp. 285-291 ◽  
Author(s):  
Masaya Sugiyama ◽  
Yasuhito Tanaka ◽  
Fuat Kurbanov ◽  
Nobuaki Nakayama ◽  
Satoshi Mochida ◽  
...  

Genes ◽  
2019 ◽  
Vol 10 (3) ◽  
pp. 182 ◽  
Author(s):  
Heléne Norder ◽  
Theogene Twagirumugabe ◽  
Joanna Said ◽  
Yarong Tian ◽  
Ka-Wei Tang ◽  
...  

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.


1996 ◽  
Vol 49 (2) ◽  
pp. 115-123 ◽  
Author(s):  
Masayuki Kurosaki ◽  
Nobuyuki Enomoto ◽  
Yasuhiro Asahina ◽  
Ikuo Sakuma ◽  
Takaaki Ikeda ◽  
...  

Virology ◽  
1991 ◽  
Vol 184 (1) ◽  
pp. 242-252 ◽  
Author(s):  
Chen Liu ◽  
Lynn D. Condreay ◽  
John B.E. Burch ◽  
William Mason

1993 ◽  
Vol 13 (1) ◽  
pp. 443-448 ◽  
Author(s):  
W Guo ◽  
M Chen ◽  
T S Yen ◽  
J H Ou

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.


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