Document Detail

Analysis of the contributions of herpes simplex virus type 1 membrane proteins to the induction of cell-cell fusion.
MedLine Citation:
PMID:  7933147     Owner:  NLM     Status:  MEDLINE    
The contributions of a set of herpes simplex virus type 1 membrane proteins towards the process of cell-cell fusion were examined with a series of deletion mutants into which a syncytial mutation had been introduced at codon 855 of the glycoprotein B (gB) gene. Analysis of the fusion phenotypes of these recombinant viruses in Vero cells revealed that while gC, gG, US5, and UL43 are dispensable for syncytium formation at both high and low multiplicities of infection, gD, gHgL, gE, gI, and gM were all required for the fusion of cellular membranes. These data confirm that the requirements for virion entry and cell-cell fusion are not identical. gD and gHgL, like gB, are essential for both processes. gG, gI, and gM, on the other hand, are dispensable for virus penetration, yet play a role in cell-to-cell spread by the direct contact route, at least on an SC16 gBANG background.
N Davis-Poynter; S Bell; T Minson; H Browne
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of virology     Volume:  68     ISSN:  0022-538X     ISO Abbreviation:  J. Virol.     Publication Date:  1994 Nov 
Date Detail:
Created Date:  1994-11-17     Completed Date:  1994-11-17     Revised Date:  2010-08-25    
Medline Journal Info:
Nlm Unique ID:  0113724     Medline TA:  J Virol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  7586-90     Citation Subset:  IM    
Department of Pathology, University of Cambridge, United Kingdom.
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MeSH Terms
Cell Membrane / virology
Cercopithecus aethiops
Herpesvirus 1, Human / physiology*
Vero Cells
Viral Envelope Proteins / genetics,  physiology*
Virion / physiology
Grant Support
//Wellcome Trust
Reg. No./Substance:
0/Viral Envelope Proteins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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