Structural and Mechanistic Insights into the Tropism of Epstein-Barr Virus

Britta S. Möhl, Jia Chen, Karthik Sathiyamoorthy, Theodore S. Jardetzky, Richard Longnecker*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

34 Scopus citations


Epstein-Barr virus (EBV) is the prototypical γ-herpesvirus and an obligate human pathogen that infects mainly epithelial cells and B cells, which can result in malignancies. EBV infects these target cells by fusing with the viral and cellular lipid bilayer membranes using multiple viral factors and host receptor(s) thus exhibiting a unique complexity in its entry machinery. To enter epithelial cells, EBV requires minimally the conserved core fusion machinery comprised of the glycoproteins gH/gL acting as the receptor- binding complex and gB as the fusogen. EBV can enter B cells using gp42, which binds tightly to gH/gL and interacts with host HLA class II, activating fusion. Previously, we published the individual crystal structures of EBV entry factors, such as gH/gL and gp42, the EBV/host receptor complex, gp42/HLA-DR1, and the fusion protein EBV gB in a postfusion conformation, which allowed us to identify structural determinants and regions critical for receptorbinding and membrane fusion. Recently, we reported different low resolution models of the EBV B cell entry triggering complex (gHgL/gp42/HLA class II) in "open" and "closed" states based on negative-stain single particle electron microscopy, which provide further mechanistic insights. This review summarizes the current knowledge of these key players in EBV entry and how their structures impact receptor- binding and the triggering of gB-mediated fusion.

Original languageEnglish (US)
Pages (from-to)286-291
Number of pages6
JournalMolecules and Cells
Issue number4
StatePublished - Apr 1 2016


  • Entry
  • Epstein-barr virus
  • Fusion
  • Herpesvirus
  • Tropism

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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