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 Turk, S. M.
Right arrow Articles by Hutt-Fletcher, L. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Turk, S. M.
Right arrow Articles by Hutt-Fletcher, L. M.

 Previous Article  |  Next Article 

Journal of Virology, October 2006, p. 9628-9633, Vol. 80, No. 19
0022-538X/06/$08.00+0     doi:10.1128/JVI.00622-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Antibodies to gp350/220 Enhance the Ability of Epstein-Barr Virus To Infect Epithelial Cells

Susan M. Turk, Ru Jiang, Liudmila S. Chesnokova, and Lindsey M. Hutt-Fletcher*

Department of Microbiology and Immunology, Center for Molecular and Tumor Virology and Feist-Weiller Cancer Center, Louisiana State University Health Sciences Center, Shreveport, Louisiana

Received 28 March 2006/ Accepted 20 July 2006

Epstein-Barr virus (EBV) is a persistent, orally transmitted herpesvirus that replicates in B cells and epithelial cells and is associated with lymphoid and epithelial malignancies. The virus binds to CD21 on B cells via glycoprotein gp350/220 and infects efficiently. Infection of cultured epithelial cells has not typically been efficient but can occur in the absence of gp350/220 and CD21 and in vivo is thought to be important to the development of nasopharyngeal carcinoma. We report here that antibodies to gp350/220, which inhibit EBV infection of B cells, enhance infection of epithelial cells. The effect is not mediated by Fc receptor binding but is further enhanced by antibody cross-linking, which may patch gp350/220 in the virus envelope. Saliva from EBV-seropositive individuals has similar effects that can be reversed by depletion of antibody. The results are consistent with a model in which gp350/220 interferes with the access of other important players to the epithelial cell surface. The results may have implications for the development of nasopharyngeal carcinoma in high-risk populations in which elevated titers of antibody to EBV lytic cycle proteins are prognostic.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Louisiana State University Health Sciences Center, Shreveport, LA 71130. Phone: (318) 675-4948. Fax: (318) 675-5764. E-mail: lhuttf{at}lsuhsc.edu.

Journal of Virology, October 2006, p. 9628-9633, Vol. 80, No. 19
0022-538X/06/$08.00+0     doi:10.1128/JVI.00622-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Sorem, J., Jardetzky, T. S., Longnecker, R. (2009). Cleavage and Secretion of Epstein-Barr Virus Glycoprotein 42 Promote Membrane Fusion with B Lymphocytes. J. Virol. 83: 6664-6672 [Abstract] [Full Text]  
  • Hutt-Fletcher, L. M. (2007). Epstein-Barr Virus Entry. J. Virol. 81: 7825-7832 [Full Text]  
  • Gaudreault, E., Fiola, S., Olivier, M., Gosselin, J. (2007). Epstein-Barr Virus Induces MCP-1 Secretion by Human Monocytes via TLR2. J. Virol. 81: 8016-8024 [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»