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 Mo, C.
Right arrow Articles by Arvin, A. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mo, C.
Right arrow Articles by Arvin, A. M.

 Previous Article  |  Next Article 

Journal of Virology, December 2000, p. 11377-11387, Vol. 74, No. 23
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Glycoprotein E of Varicella-Zoster Virus Enhances Cell-Cell Contact in Polarized Epithelial Cells

Chengjun Mo,1,* Eveline E. Schneeberger,2 and Ann M. Arvin1

Department of Pediatrics, Stanford University School of Medicine, Stanford, California 94305,1 and Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts 021142

Received 19 June 2000/Accepted 7 September 2000

Varicella-zoster virus (VZV) infection involves the cell-cell spread of virions, but how viral proteins interact with the host cell membranes that comprise intercellular junctions is not known. Madin-Darby canine kidney (MDCK) cells were constructed to express the glycoproteins gE, gI, or gE/gI constitutively and were used to examine the effects of these VZV glycoproteins in polarized epithelial cells. At low cell density, VZV gE induced partial tight junction (TJ) formation under low-calcium conditions, whether expressed alone or with gI. Although most VZV gE was intracellular, gE was also shown to colocalize with the TJ protein ZO-1 with or without concomitant expression of gI. Freeze fracture electron microscopy revealed normal TJ strand morphology in gE-expressing MDCK cells. Functionally, the expression of gE was associated with a marked acceleration in the establishment of maximum transepithelial electrical resistance (TER) in MDCK-gE cells; MDCK-gI and MDCK-gE/gI cells exhibited a similar pattern of early TER compared to MDCK cells, although peak resistances were lower than those of gE alone. VZV gE expression altered F-actin organization and lipid distribution, but coexpression of gI modulated these effects. Two regions of the gE ectodomain, amino acids (aa) 278 to 355 and aa 467 to 498, although lacking Ca2+ binding motifs, exhibit similarities with corresponding regions of the cell adhesion molecules, E-cadherin and desmocollin. These observations suggest that VZV gE and gE/gI may contribute to viral pathogenesis by facilitating epithelial cell-cell contacts.

* Corresponding author. Mailing address: G-312, Stanford University School of Medicine, 300 Pasteur Dr., Stanford, CA 94305. Phone: (650) 725-6555. Fax: (650) 725-8040. E-mail: cmo{at}cmgm.stanford.edu.

Journal of Virology, December 2000, p. 11377-11387, Vol. 74, No. 23
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Reichelt, M., Brady, J., Arvin, A. M. (2009). The Replication Cycle of Varicella-Zoster Virus: Analysis of the Kinetics of Viral Protein Expression, Genome Synthesis, and Virion Assembly at the Single-Cell Level. J. Virol. 83: 3904-3918 [Abstract] [Full Text]  
  • Berarducci, B., Rajamani, J., Reichelt, M., Sommer, M., Zerboni, L., Arvin, A. M. (2009). Deletion of the First Cysteine-Rich Region of the Varicella-Zoster Virus Glycoprotein E Ectodomain Abolishes the gE and gI Interaction and Differentially Affects Cell-Cell Spread and Viral Entry. J. Virol. 83: 228-240 [Abstract] [Full Text]  
  • Zerboni, L., Reichelt, M., Jones, C. D., Zehnder, J. L., Ito, H., Arvin, A. M. (2007). From the Cover: Aberrant infection and persistence of varicella-zoster virus in human dorsal root ganglia in vivo in the absence of glycoprotein I. Proc. Natl. Acad. Sci. USA 104: 14086-14091 [Abstract] [Full Text]  
  • Li, Q., Krogmann, T., Ali, M. A., Tang, W.-J., Cohen, J. I. (2007). The Amino Terminus of Varicella-Zoster Virus (VZV) Glycoprotein E Is Required for Binding to Insulin-Degrading Enzyme, a VZV Receptor. J. Virol. 81: 8525-8532 [Abstract] [Full Text]  
  • Berarducci, B., Ikoma, M., Stamatis, S., Sommer, M., Grose, C., Arvin, A. M. (2006). Essential Functions of the Unique N-Terminal Region of the Varicella-Zoster Virus Glycoprotein E Ectodomain in Viral Replication and in the Pathogenesis of Skin Infection. J. Virol. 80: 9481-9496 [Abstract] [Full Text]  
  • Moffat, J., Mo, C., Cheng, J. J., Sommer, M., Zerboni, L., Stamatis, S., Arvin, A. M. (2004). Functions of the C-Terminal Domain of Varicella-Zoster Virus Glycoprotein E in Viral Replication In Vitro and Skin and T-Cell Tropism In Vivo. J. Virol. 78: 12406-12415 [Abstract] [Full Text]  
  • Besser, J., Sommer, M. H., Zerboni, L., Bagowski, C. P., Ito, H., Moffat, J., Ku, C.-C., Arvin, A. M. (2003). Differentiation of Varicella-Zoster Virus ORF47 Protein Kinase and IE62 Protein Binding Domains and Their Contributions to Replication in Human Skin Xenografts in the SCID-hu Mouse. J. Virol. 77: 5964-5974 [Abstract] [Full Text]  
  • Kenyon, T. K., Cohen, J. I., Grose, C. (2002). Phosphorylation by the Varicella-Zoster Virus ORF47 Protein Serine Kinase Determines whether Endocytosed Viral gE Traffics to the trans-Golgi Network or Recycles to the Cell Membrane. J. Virol. 76: 10980-10993 [Abstract] [Full Text]  
  • Law, M., Hollinshead, R., Smith, G. L. (2002). Antibody-sensitive and antibody-resistant cell-to-cell spread by vaccinia virus: role of the A33R protein in antibody-resistant spread. J. Gen. Virol. 83: 209-222 [Abstract] [Full Text]  
  • Schumacher, D., Tischer, B. K., Reddy, S. M., Osterrieder, N. (2001). Glycoproteins E and I of Marek's Disease Virus Serotype 1 Are Essential for Virus Growth in Cultured Cells. J. Virol. 75: 11307-11318 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»