scholarly journals Hepatitis B virus X protein promotes human hepatoma cell growth via upregulation of transcription factor AP2α and sphingosine kinase 1

2015 ◽  
Vol 36 (10) ◽  
pp. 1228-1236 ◽  
Author(s):  
Zhan-ping Lu ◽  
Ze-lin Xiao ◽  
Zhe Yang ◽  
Jiong Li ◽  
Guo-xing Feng ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Hepatitis B Virus ◽  
Cell Growth ◽  
Hepatitis B ◽  
Hepatoma Cell ◽  
Sphingosine Kinase ◽  
Human Hepatoma ◽  
Sphingosine Kinase 1 ◽  
Human Hepatoma Cell ◽  
B Virus

scholarly journals Transfection of N-Acetylglucosaminyltransferase III Gene Suppresses Expression of Hepatitis B Virus in a Human Hepatoma Cell Line, HB611

1995 ◽  
Vol 270 (47) ◽  
pp. 28311-28315 ◽  
Author(s):  
Eiji Miyoshi ◽  
Yoshito Ihara ◽  
Norio Hayashi ◽  
Hideyuki Fusamoto ◽  
Takenobu Kamada ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Cell Line ◽  
Hepatoma Cell ◽  
Hepatoma Cell Line ◽  
Human Hepatoma ◽  
Human Hepatoma Cell ◽  
Human Hepatoma Cell Line ◽  
B Virus

Chemokine Expression Profiles of Human Hepatoma Cell Lines Mediated by Hepatitis B Virus X Protein

2015 ◽  
Vol 22 (2) ◽  
pp. 393-399 ◽  
Author(s):  
Di-Yi Wang ◽  
Li-Ping Zou ◽  
Xiao-Jia Liu ◽  
Hong-Guang Zhu ◽  
Rong Zhu
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Cell Lines ◽  
Expression Profiles ◽  
Hepatoma Cell ◽  
Human Hepatoma ◽  
X Protein ◽  
Human Hepatoma Cell ◽  
Hepatoma Cell Lines ◽  
B Virus

Hepatitis B Virus e Antigen Downregulates Cytokine Production in Human Hepatoma Cell Lines

2010 ◽  
Vol 23 (5) ◽  
pp. 467-476 ◽  
Author(s):  
Shuang Wu ◽  
Tatsuo Kanda ◽  
Fumio Imazeki ◽  
Makoto Arai ◽  
Yutaka Yonemitsu ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Cell Lines ◽  
Cytokine Production ◽  
Hepatoma Cell ◽  
Human Hepatoma ◽  
Human Hepatoma Cell ◽  
Hepatoma Cell Lines ◽  
B Virus

scholarly journals Stable expression and integrated hepatitis B virus genome in a human hepatoma cell line

2012 ◽  
Vol 11 (2) ◽  
pp. 1442-1448 ◽  
Author(s):  
L.Y. Wang ◽  
Y.G. Li ◽  
K. Chen ◽  
K. Li ◽  
J.L. Qu ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Cell Line ◽  
Hepatoma Cell ◽  
Virus Genome ◽  
Stable Expression ◽  
Hepatoma Cell Line ◽  
Human Hepatoma ◽  
Human Hepatoma Cell ◽  
B Virus

scholarly journals Hepatitis B Virus (HBV) Virion and Covalently Closed Circular DNA Formation in Primary Tupaia Hepatocytes and Human Hepatoma Cell Lines upon HBV Genome Transduction with Replication-Defective Adenovirus Vectors

2001 ◽  
Vol 75 (3) ◽  
pp. 1104-1116 ◽  
Author(s):  
Shaotang Ren ◽  
Michael Nassal
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Hepatoma Cell ◽  
Human Hepatoma ◽  
Human Hepatoma Cell ◽  
Hepatoma Cell Lines ◽  
Animal System ◽  
B Virus ◽  
Adenovirus Vectors ◽  
Replication Defective Adenovirus

ABSTRACT Hepatitis B virus (HBV), the causative agent of B-type hepatitis in humans, is a hepatotropic DNA-containing virus that replicates via reverse transcription. Because of its narrow host range, there is as yet no practical small-animal system for HBV infection. The hosts of the few related animal viruses, including woodchuck hepatitis B virus and duck hepatitis B virus, are either difficult to keep or only distantly related to humans. Some evidence suggests that tree shrews (tupaias) may be susceptible to infection with human HBV, albeit with low efficiency. Infection efficiency depends on interactions of the virus with factors on the surface and inside the host cell. To bypass restrictions during the initial entry phase, we used recombinant replication-defective adenovirus vectors, either with or without a green fluorescent protein marker gene, to deliver complete HBV genomes into primary tupaia hepatocytes. Here we show that these cells, like the human hepatoma cell lines HepG2 and Huh7, are efficiently transduced by the vectors and produce all HBV gene products required to generate the secretory antigens HBsAg and HBeAg, replication-competent nucleocapsids, and enveloped virions. We further demonstrate that covalently closed circular HBV DNA is formed. Therefore, primary tupaia hepatocytes support all steps of HBV replication following deposition of the genome in the nucleus, including the intracellular amplification cycle. These data provide a rational basis for in vivo experiments aimed at developing tupaias into a useful experimental animal system for HBV infection.

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