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Journal of Virology, September 2005, p. 10923-10930, Vol. 79, No. 17
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.17.10923-10930.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Mutations of Epstein-Barr Virus gH That Are Differentially Able To Support Fusion with B Cells or Epithelial Cells

Liguo Wu,1,2 Corina M. Borza,1,{dagger} and Lindsey M. Hutt-Fletcher1,2*

School of Biological Sciences, University of Missouri—Kansas City, Kansas City, Missouri,1 Department of Microbiology and Immunology, Center for Molecular and Tumor Virology, and Feist-Weiller Cancer Center, Louisiana State University Health Sciences Center, Shreveport, Louisiana2

Received 8 April 2005/ Accepted 26 May 2005

The core fusion machinery of all herpesviruses consists of three conserved glycoproteins, gB and gHgL, suggesting a common mechanism for virus cell fusion, but fusion of Epstein-Barr virus (EBV) with B cells and epithelial cells is initiated differently. Fusion with B cells requires a fourth protein, gp42, which complexes with gHgL and interacts with HLA class II, the B-cell coreceptor. Fusion with an epithelial cell does not require gp42 but requires interaction of gHgL with a novel epithelial cell coreceptor. Epithelial cell fusion can be inhibited by gp42 binding to gHgL and by antibodies to gH that fail to block B-cell fusion. This suggests that regions of gHgL initiating fusion with each cell are separable from each other and from regions involved in fusion itself. To address this possibility we mapped the region of gH recognized by a monoclonal antibody to gH that blocks EBV fusion with epithelial cells but not B cells by making a series of chimeras with the gH homolog of rhesus lymphocryptovirus. Proteins with mutations engineered within this region included those that preferentially mediate fusion with B cells, those that preferentially mediate fusion with epithelial cells, and those that mediate fusion with neither cell type. These results support the hypothesis that the core fusion function of gH is the same for B cells and epithelial cells and that it differs only in the way in which it is triggered into a functionally active state.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Louisiana State University Health Sciences Center, 1501 Kings Highway, Shreveport, LA 71130. Phone: (318) 675-4948. Fax: (318) 675-5764. E-mail: lhuttf{at}lsuhsc.edu.

{dagger} Present address: Division of Nephrology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232.

Journal of Virology, September 2005, p. 10923-10930, Vol. 79, No. 17
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.17.10923-10930.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Kirschner, A. N., Lowrey, A. S., Longnecker, R., Jardetzky, T. S. (2007). Binding-Site Interactions between Epstein-Barr Virus Fusion Proteins gp42 and gH/gL Reveal a Peptide That Inhibits both Epithelial and B-Cell Membrane Fusion. J. Virol. 81: 9216-9229 [Abstract] [Full Text]  
  • Wu, L., Hutt-Fletcher, L. M. (2007). Compatibility of the gH homologues of Epstein-Barr virus and related lymphocryptoviruses. J. Gen. Virol. 88: 2129-2136 [Abstract] [Full Text]  
  • Hutt-Fletcher, L. M. (2007). Epstein-Barr Virus Entry. J. Virol. 81: 7825-7832 [Full Text]  


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