Mutations in herpes simplex virus glycoprotein D distinguish entry of free virus from cell-cell spread

D. A. Rauch, N. Rodriguez, R. J. Roller

Research output: Contribution to journalArticlepeer-review

30 Scopus citations

Abstract

Herpes simplex virus type 1 (HSV-1) glycoprotein D (gD) is an essential component of the entry apparatus that is responsible for viral penetration and subsequent cell-cell spread. To test the hypothesis that gD may serve distinguishable functions in entry of free virus and cell-cell spread, mutants were selected for growth on Us11c119.3 cells, which are resistant to both processes due to the lack of a functional gD receptor, and then tested for their ability to enter as free virus and to spread from cell to cell. Unlike their wild-type parent, HSV-1(F), the variants that emerged from this selection, which were named SP mutants, are all capable of forming macroscopic plaques on the resistant cells. This ability is caused by a marked increase in cell-cell spread without a concomitant increase in efficiency of entry of free virus. gD substitutions that arose within these mutants are sufficient to mediate cell-cell spread in Us11c119.3 cells but are insufficient to overcome the restriction to entry of free virions. These results suggest that mutations in gD (i) are sufficient but not necessary to overcome the block to cell-cell spread exhibited by Us11c119.3 cells and (ii) are insufficient to mediate entry of free virus in the same cells.

Original languageEnglish
Pages (from-to)11437-11446
Number of pages10
JournalJournal of virology
Volume74
Issue number24
DOIs
StatePublished - 2000

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