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 Finnen, R. L.
Right arrow Articles by Levin, M. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Finnen, R. L.
Right arrow Articles by Levin, M. J.

 Previous Article  |  Next Article 

Journal of Virology, November 2006, p. 10325-10334, Vol. 80, No. 21
0022-538X/06/$08.00+0     doi:10.1128/JVI.00939-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Postentry Events Are Responsible for Restriction of Productive Varicella-Zoster Virus Infection in Chinese Hamster Ovary Cells

Renée L. Finnen,1* Kara R. Mizokami,1 Bruce W. Banfield,2 Guang-Yun Cai,1 Scott A. Simpson,1 Lewis I. Pizer,1,2 and Myron J. Levin1

Department of Pediatrics, Infectious Diseases Section,1 Department of Microbiology, University of Colorado Health Sciences Center, Denver, Colorado 802622

Received 9 May 2006/ Accepted 7 August 2006

Productive infection of varicella-zoster virus (VZV) in vitro is restricted almost exclusively to cells derived from humans and other primates. We demonstrate that the restriction of productive VZV infection in CHO-K1 cells occurs downstream of virus entry. Entry of VZV into CHO-K1 cells was characterized by utilizing an ICP4/ß-galactosidase reporter gene that has been used previously to study herpes simplex virus type 1 entry. Entry of VZV into CHO-K1 cells involved cell surface interactions with heparan sulfate glycosaminoglycans and a cation-independent mannose-6-phosphate receptor. Lysosomotropic agents inhibited the entry of VZV into CHO-K1 cells, consistent with a low-pH-dependent endocytic mechanism of entry. Infection of CHO-K1 cells by VZV resulted in the production of both immediate early and late gene products, indicating that a block to progeny virus production occurs after the initiation of virus gene expression.


* Corresponding author. Mailing address: Department of Pediatrics, Infectious Diseases Section, Biomedical Research Building 851, C227, University of Colorado Health Sciences Center, 4200 East Ninth Avenue, Denver, CO 80262. Phone: (303) 315-4183. Fax: (303) 315-7909. E-mail: renee.finnen{at}uchsc.edu.


Journal of Virology, November 2006, p. 10325-10334, Vol. 80, No. 21
0022-538X/06/$08.00+0     doi:10.1128/JVI.00939-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Coletta, R. D., Christensen, K. L., Micalizzi, D. S., Jedlicka, P., Varella-Garcia, M., Ford, H. L. (2008). Six1 Overexpression in Mammary Cells Induces Genomic Instability and Is Sufficient for Malignant Transformation. Cancer Res. 68: 2204-2213 [Abstract] [Full Text]  
  • Hambleton, S., Steinberg, S. P., Gershon, M. D., Gershon, A. A. (2007). Cholesterol Dependence of Varicella-Zoster Virion Entry into Target Cells. J. Virol. 81: 7548-7558 [Abstract] [Full Text]