Literature DB >> 2777207

Replication of duck hepatitis B virus in primary duck hepatocytes and its dependence on the state of differentiation of the host cell.

P R Galle1, H J Schlicht, C Kuhn, H Schaller.   

Abstract

Primary duck hepatocytes obtained from Pekin ducks congenitally infected with duck hepatitis B virus were used to monitor expression of viral proteins and replication of viral DNA in cell culture. Duck hepatitis B virus core antigen, duck hepatitis B virus pre-surface antigen and duck hepatitis B virus DNA were detectable for at least 12 days after cell plating. Whereas expression of duck hepatitis B pre-surface antigen was constant during this time, expression of duck hepatitis B core antigen and of viral DNA rapidly declined. This diminished production of viral components in vitro was paralleled by a change of the hepatocytes toward a fibroblast-like morphology. Supplementation of cell culture medium with 2% dimethyl sulfoxide, a solvent known to maintain the differentiated state of cultured cells, retained competence of the cultured hepatocytes to express duck hepatitis B core antigen and duck hepatitis B virus DNA at high levels. In a second set of experiments, duck hepatitis B virus negative hepatocytes were infected with duck hepatitis B virus from serum of congenitally infected ducks. Dimethyl sulfoxide remarkably improved the competence of cultured duck hepatocytes to become productively infected. This function was maintained for at least 12 days postplating.

Entities:  

Mesh:

Substances:

Year:  1989        PMID: 2777207     DOI: 10.1002/hep.1840100410

Source DB:  PubMed          Journal:  Hepatology        ISSN: 0270-9139            Impact factor:   17.425


  12 in total

1.  Replication advantage and host factor-independent phenotypes attributable to a common naturally occurring capsid mutation (I97L) in human hepatitis B virus.

Authors:  Fat-Moon Suk; Min-Hui Lin; Margaret Newman; Shann Pan; Sheng-Hsuan Chen; Jean-Dean Liu; Chiaho Shih
Journal:  J Virol       Date:  2002-12       Impact factor: 5.103

Review 2.  Viral and cellular determinants involved in hepadnaviral entry.

Authors:  Dieter Glebe; Stephan Urban
Journal:  World J Gastroenterol       Date:  2007-01-07       Impact factor: 5.742

3.  Endotoxin stimulates liver macrophages to release mediators that inhibit an early step in hepadnavirus replication.

Authors:  U Klöcker; U Schultz; H Schaller; U Protzer
Journal:  J Virol       Date:  2000-06       Impact factor: 5.103

4.  Analysis of the earliest steps of hepadnavirus replication: genome repair after infectious entry into hepatocytes does not depend on viral polymerase activity.

Authors:  J Köck; H J Schlicht
Journal:  J Virol       Date:  1993-08       Impact factor: 5.103

5.  Duck hepatitis B virus infection of hepatocytes is not dependent on low pH.

Authors:  R J Rigg; H Schaller
Journal:  J Virol       Date:  1992-05       Impact factor: 5.103

6.  Transfer of hepatitis B virus genome by adenovirus vectors into cultured cells and mice: crossing the species barrier.

Authors:  M F Sprinzl; H Oberwinkler; H Schaller; U Protzer
Journal:  J Virol       Date:  2001-06       Impact factor: 5.103

7.  Glucagon treatment interferes with an early step of duck hepatitis B virus infection.

Authors:  M Hild; O Weber; H Schaller
Journal:  J Virol       Date:  1998-04       Impact factor: 5.103

8.  Regulatory sequences of duck hepatitis B virus C gene transcription.

Authors:  R Schneider; H Will
Journal:  J Virol       Date:  1991-11       Impact factor: 5.103

Review 9.  Is hepatitis B-virucidal validation of biocides possible with the use of surrogates?

Authors:  Andreas Sauerbrei
Journal:  World J Gastroenterol       Date:  2014-01-14       Impact factor: 5.742

10.  Hepadnavirus infection requires interaction between the viral pre-S domain and a specific hepatocellular receptor.

Authors:  U Klingmüller; H Schaller
Journal:  J Virol       Date:  1993-12       Impact factor: 5.103

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.