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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.
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.
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