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Journal of Virology, October 2006, p. 9544-9556, Vol. 80, No. 19
0022-538X/06/$08.00+0     doi:10.1128/JVI.00668-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Delayed Biosynthesis of Varicella-Zoster Virus Glycoprotein C: Upregulation by Hexamethylene Bisacetamide and Retinoic Acid Treatment of Infected Cells

Johnathan Storlie, Wallen Jackson, Jennifer Hutchinson, and Charles Grose*

Departments of Microbiology and Pediatrics, University of Iowa College of Medicine, Iowa City, Iowa 52242

Received 3 April 2006/ Accepted 11 July 2006

In the course of examining the trafficking pathways of varicella-zoster virus (VZV) glycoproteins gE, gI, gH, and gB, we discovered that all four are synthesized within 4 to 6 h postinfection (hpi) in cultured cells. Thereafter, they travel via the trans-Golgi network to the outer cell membrane. When we carried out a similar analysis on VZV gC, we observed little gC biosynthesis in the first 72 hpi. Further examination disclosed that gC was present in the inocula of infected cells, but no new gC biosynthesis occurred during the first 24 to 48 h thereafter, during which time new synthesis of gE, gH, and major capsid protein was easily detectable. Similarly, delayed gC biosynthesis was confirmed with three different VZV strains and two different cell lines. Bioinformatics analyses disclosed the presence of PBX/HOX consensus binding domains in the promoter/enhancer regions of the genes for VZV gC and ORF4 protein (whose orthologs transactivate gC in other herpesviruses). Bioinformatics analysis also identified two HOXA9 activation regions on ORF4 protein. Treatment of infected cultures with chemicals known to induce the production of PBX/HOX transcription proteins, namely, hexamethylene bisacetamide (HMBA) and retinoic acid, led to more rapid gC biosynthesis. Immunoblotting demonstrated a fivefold increase in the HOXA9 protein after HMBA treatment. In summary, these results documented that gC was not produced during early VZV replication cycles, presumably related to a deficiency in the PBX/HOX transcription factors. Furthermore, these results explain the apparent spontaneous loss of VZV gC in some passaged viruses, as well as other anomalous gC results.

* Corresponding author. Mailing address: University Hospital/2501 JCP, 200 Hawkins Dr., Iowa City, IA 52242. Phone: (319) 356-2270. Fax: (319) 356-4855. E-mail: charles-grose{at}uiowa.edu.

Journal of Virology, October 2006, p. 9544-9556, Vol. 80, No. 19
0022-538X/06/$08.00+0     doi:10.1128/JVI.00668-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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