Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-3-29
pubmed:abstractText
Several human and animal alphaherpesviruses can enter cells via human herpesvirus entry mediator C (HveC), a receptor for viral glycoprotein D (gD). In previous studies with cells expressing unknown entry mediators, cellular expression of alphaherpesvirus gD was shown to inhibit entry of the homologous virus and sometimes also of heterologous alphaherpesviruses. To investigate the mechanism of gD-mediated interference and the basis for cross-interference among alphaherpesviruses, HveC was expressed in cells as the sole entry mediator, in the presence or absence of one of the gDs encoded by herpes simplex virus type 1, pseudorabies virus, or bovine herpesvirus type 1. Cells expressing HveC alone were highly susceptible to entry of all three viruses, whereas cells coexpressing HveC and any one of the gDs were at least partially resistant to infection by each virus. Coexpression of gD with HveC did not cause reduced levels of cell-surface HveC but the HveC had reduced ability to bind to exogenous gD. Coimmunoprecipitation experiments revealed that HveC was complexed with gD in lysates of cells expressing both. Thus, cellular expression of gD can interfere with alphaherpesvirus entry by blocking ligand-binding sites of the gD receptor(s) used for entry and cross-interference can occur because different forms of alphaherpesvirus gD can compete for shared entry receptors.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0042-6822
pubmed:author
pubmed:copyrightInfo
Copyright 2000 Academic Press.
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
268
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
147-58
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Cellular expression of alphaherpesvirus gD interferes with entry of homologous and heterologous alphaherpesviruses by blocking access to a shared gD receptor.
pubmed:affiliation
Department of Microbiology-Immunology, Northwestern University Medical School, Chicago, Illinois, 60611, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.