The requirements for herpes simplex virus type 1 cell-cell spread via nectin-1 parallel those for virus entry

Deborah L. Even, Allison M. Henley, Robert J. Geraghty

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

Herpes simplex virus type 1 (HSV-1) spreads from an infected cell to an uninfected cell by virus entry, virus-induced cell fusion, and cell-cell spread. The three forms of virus spread require the viral proteins gB, gD, and gH-gL, as well as a cellular gD receptor. The mutual requirement for the fusion glycoproteins and gD receptor suggests that virus entry, cell fusion, and cell-cell spread occur by a similar mechanism. The goals of this study were to examine the role of the nectin-1α transmembrane domain and cytoplasmic tail in cell-cell spread and to obtain a better understanding of the receptor-dependent events occurring at the plasma membrane during cell-cell spread. We determined that an intact nectin-1α V-like domain was required for cell-cell spread, while a membrane-spanning domain and cytoplasmic tail were not. Chimeric forms of nectin-1 that were non-functional for virus entry did not mediate cell-cell spread regardless of whether they could mediate cell fusion. Also, cell-cell spread of syncytial isolates was dependent upon nectin-1α expression and occurred through a nectin-1-dependent mechanism. Taken together, our results indicate that nectin-1-dependent events occurring at the plasma membrane during cell-cell spread were equivalent to those for virus entry.

Original languageEnglish (US)
Pages (from-to)195-207
Number of pages13
JournalVirus research
Volume119
Issue number2
DOIs
StatePublished - Aug 1 2006
Externally publishedYes

Keywords

  • Cell fusion
  • Cell-cell spread
  • Herpes simplex virus
  • Nectin-1
  • Virus entry

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