This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Sainz, B.
Right arrow Articles by Chisari, F. V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sainz, B., Jr.
Right arrow Articles by Chisari, F. V.

 Previous Article  |  Next Article 

Journal of Virology, October 2006, p. 10253-10257, Vol. 80, No. 20
0022-538X/06/$08.00+0     doi:10.1128/JVI.01059-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Production of Infectious Hepatitis C Virus by Well-Differentiated, Growth-Arrested Human Hepatoma-Derived Cells{dagger}

Bruno Sainz Jr. and Francis V. Chisari*

Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037

Received 23 May 2006/ Accepted 31 July 2006

Dimethyl sulfoxide (DMSO) has been shown to induce the differentiation of primary hepatocytes in vitro. When actively dividing poorly differentiated human hepatoma-derived (Huh7) cells were cultured in the presence of 1% DMSO, cells became cytologically differentiated and transitioned into a nondividing state, characterized by the induction of hepatocyte-specific genes. Moreover, these cells were highly permissive for acute hepatitis C virus (HCV) infection, and persistent long term infection of these cultures could also be achieved. As HCV naturally replicates in highly differentiated nondividing human hepatocytes, this system may more accurately mimic the conditions under which HCV replicates in vivo than previous models using poorly differentiated rapidly dividing hepatoma cells.


* Corresponding author. Mailing address: Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, SBR-10, La Jolla, CA 92037. Phone: (858) 784-8228. Fax: (858) 784-2160. E-mail: fchisari{at}scripps.edu.

{dagger} This is manuscript number 18185-MEM from The Scripps Research Institute.


Journal of Virology, October 2006, p. 10253-10257, Vol. 80, No. 20
0022-538X/06/$08.00+0     doi:10.1128/JVI.01059-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Cheng, G., Montero, A., Gastaminza, P., Whitten-Bauer, C., Wieland, S. F., Isogawa, M., Fredericksen, B., Selvarajah, S., Gallay, P. A., Ghadiri, M. R., Chisari, F. V. (2008). A virocidal amphipathic {alpha}-helical peptide that inhibits hepatitis C virus infection in vitro. Proc. Natl. Acad. Sci. USA 105: 3088-3093 [Abstract] [Full Text]  
  • Zhong, J., Gastaminza, P., Chung, J., Stamataki, Z., Isogawa, M., Cheng, G., McKeating, J. A., Chisari, F. V. (2006). Persistent Hepatitis C Virus Infection In Vitro: Coevolution of Virus and Host. J. Virol. 80: 11082-11093 [Abstract] [Full Text]