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 language | English (US) |
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Pages (from-to) | 195-207 |
Number of pages | 13 |
Journal | Virus research |
Volume | 119 |
Issue number | 2 |
DOIs | |
State | Published - Aug 2006 |
Externally published | Yes |
Bibliographical note
Funding Information:This investigation was funded by a National Institutes of Health Grant #AI51476.
Keywords
- Cell fusion
- Cell-cell spread
- Herpes simplex virus
- Nectin-1
- Virus entry