Mutations in the cytoplasmic tail of herpes simplex virus glycoprotein H suppress cell fusion by a syncytial strain

Duncan W. Wilson, Nick Davis-Poynter, Anthony C. Minson

Research output: Contribution to journalArticle

63 Citations (Scopus)

Abstract

We have developed a complementation assay, using transiently transfected COS cells, to facilitate a molecular analysis of the herpes simplex virus type 1 glycoprotein gH. When infected by a gH-null syncytial virus, COS cells expressing wild-type gH generate infectious progeny virions and form a syncytium with neighboring cells. By deletion and point mutagenesis, we have found particular residues in the gH cytoplasmic tail to be essential for generation of a syncytium but apparently dispensable for production of infectious virions. This study emphasizes the different requirements for cell-cell and cell-envelope fusion and demonstrates that changes in the non- syn locus UL22-gH can reverse the syncytial phenotype.

Original languageEnglish (US)
Pages (from-to)6985-6993
Number of pages9
JournalJournal of Virology
Volume68
Issue number11
StatePublished - Nov 1994

Fingerprint

herpes simplex
cell fusion
Cell Fusion
Simplexvirus
glycoproteins
Glycoproteins
tail
COS Cells
Giant Cells
mutation
Virion
viruses
Mutation
Human Herpesvirus 1
giant cells
cells
virion
Mutagenesis
Viruses
Phenotype

ASJC Scopus subject areas

  • Immunology

Cite this

Mutations in the cytoplasmic tail of herpes simplex virus glycoprotein H suppress cell fusion by a syncytial strain. / Wilson, Duncan W.; Davis-Poynter, Nick; Minson, Anthony C.

In: Journal of Virology, Vol. 68, No. 11, 11.1994, p. 6985-6993.

Research output: Contribution to journalArticle

@article{f263bd0b6c904304a0b51b6e972c7c1c,
title = "Mutations in the cytoplasmic tail of herpes simplex virus glycoprotein H suppress cell fusion by a syncytial strain",
abstract = "We have developed a complementation assay, using transiently transfected COS cells, to facilitate a molecular analysis of the herpes simplex virus type 1 glycoprotein gH. When infected by a gH-null syncytial virus, COS cells expressing wild-type gH generate infectious progeny virions and form a syncytium with neighboring cells. By deletion and point mutagenesis, we have found particular residues in the gH cytoplasmic tail to be essential for generation of a syncytium but apparently dispensable for production of infectious virions. This study emphasizes the different requirements for cell-cell and cell-envelope fusion and demonstrates that changes in the non- syn locus UL22-gH can reverse the syncytial phenotype.",
author = "Wilson, {Duncan W.} and Nick Davis-Poynter and Minson, {Anthony C.}",
year = "1994",
month = "11",
language = "English (US)",
volume = "68",
pages = "6985--6993",
journal = "Journal of Virology",
issn = "0022-538X",
publisher = "American Society for Microbiology",
number = "11",

}

TY - JOUR

T1 - Mutations in the cytoplasmic tail of herpes simplex virus glycoprotein H suppress cell fusion by a syncytial strain

AU - Wilson, Duncan W.

AU - Davis-Poynter, Nick

AU - Minson, Anthony C.

PY - 1994/11

Y1 - 1994/11

N2 - We have developed a complementation assay, using transiently transfected COS cells, to facilitate a molecular analysis of the herpes simplex virus type 1 glycoprotein gH. When infected by a gH-null syncytial virus, COS cells expressing wild-type gH generate infectious progeny virions and form a syncytium with neighboring cells. By deletion and point mutagenesis, we have found particular residues in the gH cytoplasmic tail to be essential for generation of a syncytium but apparently dispensable for production of infectious virions. This study emphasizes the different requirements for cell-cell and cell-envelope fusion and demonstrates that changes in the non- syn locus UL22-gH can reverse the syncytial phenotype.

AB - We have developed a complementation assay, using transiently transfected COS cells, to facilitate a molecular analysis of the herpes simplex virus type 1 glycoprotein gH. When infected by a gH-null syncytial virus, COS cells expressing wild-type gH generate infectious progeny virions and form a syncytium with neighboring cells. By deletion and point mutagenesis, we have found particular residues in the gH cytoplasmic tail to be essential for generation of a syncytium but apparently dispensable for production of infectious virions. This study emphasizes the different requirements for cell-cell and cell-envelope fusion and demonstrates that changes in the non- syn locus UL22-gH can reverse the syncytial phenotype.

UR - http://www.scopus.com/inward/record.url?scp=0028046624&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028046624&partnerID=8YFLogxK

M3 - Article

VL - 68

SP - 6985

EP - 6993

JO - Journal of Virology

JF - Journal of Virology

SN - 0022-538X

IS - 11

ER -