Gammaherpesvirus entry and fusion: A tale how two human pathogenic viruses enter their host cells

Britta S. Möhl*, Jia Chen, Richard Longnecker

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapter

15 Scopus citations


The prototypical human γ-herpesviruses Epstein-Barr virus (EBV) and Kaposi Sarcoma-associated herpesvirus (KSHV) are involved in the development of malignancies. Like all herpesviruses, they share the establishment of latency, the typical architecture, and the conserved fusion machinery to initiate infection. The fusion machinery reflects virus-specific adaptations due to the requirements of the respective herpesvirus. For example, EBV evolved a tropism switch involving either the B- or epithelial cell-tropism complexes to activate fusion driven by gB. Most of the EBV entry proteins and their cellular receptors have been crystallized providing molecular details of the initial steps of infection. For KSHV, a variety of entry and binding receptors has also been reported but the mechanism how receptor binding activates gB-driven fusion is not as well understood as that for EBV. However, the downstream signaling pathways that promote the early steps of KSHV entry are well described. This review summarizes the current knowledge of the key players involved in EBV and KSHV entry and the cell-type specific mechanisms that allow infection of a wide variety of cell types.

Original languageEnglish (US)
Title of host publicationVirus Entry
EditorsMargaret Kielian, Thomas C. Mettenleiter, Marilyn J. Roossinck
PublisherAcademic Press Inc
Number of pages31
ISBN (Print)9780128183946
StatePublished - 2019

Publication series

NameAdvances in Virus Research
ISSN (Print)0065-3527
ISSN (Electronic)1557-8399


  • Epstein-Barr virus (EBV)
  • Gammaherpesvirus entry and fusion
  • Glycoprotein gB and gH/gL
  • Kaposi Sarcoma-associated herpesvirus (KSHV)
  • Viral fusion
  • Virus entry

ASJC Scopus subject areas

  • Virology
  • Infectious Diseases


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