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J Virol. 2006 Nov;80(21):10325-34.

Postentry events are responsible for restriction of productive varicella-zoster virus infection in Chinese hamster ovary cells.

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  • 1Department of Pediatrics, Infectious Diseases Section, Biomedical Research Building 851, C227, University of Colorado Health Sciences Center, 4200 East Ninth Avenue, Denver, CO 80262, USA.


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/beta-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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