Stimulation of the interleukin-1 receptor and Toll-like receptor 2 inhibits hepatitis B virus replication in hepatoma cell lines in vitro

2009 ◽  
Vol 14 (6) ◽  
pp. 797-808 ◽  
Author(s):  
Alex J Thompson ◽  
Danni Colledge ◽  
Sally Rodgers ◽  
Rachel Wilson ◽  
Peter Revill ◽  
...  
1987 ◽  
Vol 6 (3) ◽  
pp. 675-680 ◽  
Author(s):  
C.M. Chang ◽  
K.S. Jeng ◽  
C.P. Hu ◽  
S.J. Lo ◽  
T.S. Su ◽  
...  

2015 ◽  
Vol 22 (2) ◽  
pp. 393-399 ◽  
Author(s):  
Di-Yi Wang ◽  
Li-Ping Zou ◽  
Xiao-Jia Liu ◽  
Hong-Guang Zhu ◽  
Rong Zhu

2010 ◽  
Vol 23 (5) ◽  
pp. 467-476 ◽  
Author(s):  
Shuang Wu ◽  
Tatsuo Kanda ◽  
Fumio Imazeki ◽  
Makoto Arai ◽  
Yutaka Yonemitsu ◽  
...  

1983 ◽  
Vol 39 (3) ◽  
pp. 1361-1367 ◽  
Author(s):  
Y M Wen ◽  
K Mitamura ◽  
B Merchant ◽  
Z Y Tang ◽  
R H Purcell

2001 ◽  
Vol 75 (3) ◽  
pp. 1104-1116 ◽  
Author(s):  
Shaotang Ren ◽  
Michael Nassal

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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