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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
Pt 11
pubmed:dateCreated
2002-10-21
pubmed:abstractText
Infection with human cytomegalovirus (HCMV) is known to involve complex interactions between viral and cellular factors resulting in perturbation of a number of cellular functions. Specifically, HCMV infection targets control of the cell cycle, cellular transcription and immunoregulation, presumably to optimize the cellular environment for virus persistence and productive infection. Here, we show that HCMV infection also prevents external signalling to the cell by disrupting the function of epidermal growth factor receptor (EGFR). Infection with HCMV resulted in a decrease in cell-surface expression of EGFR. This decrease was correlated with a concomitant decrease in steady-state levels of EGFR protein. Consistent with this, HCMV inhibited EGF-mediated receptor autophosphorylation. Infection with a mutant HCMV deleted of all viral gene products known to be involved in down-regulation of MHC Class I receptors still resulted in this down-regulation, implying that EGFR down-regulation by HCMV is mediated by a novel virus function. We suggest that a primary goal of HCMV is to 'isolate' the infected cell from host-mediated signals so that the cell responds solely to an array of virus-specific signals which optimize the cell for virus production.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-1317
pubmed:author
pubmed:issnType
Print
pubmed:volume
83
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2803-10
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Human cytomegalovirus infection inhibits epidermal growth factor (EGF) signalling by targeting EGF receptors.
pubmed:affiliation
Department of Medicine, University of Cambridge, Level 5, Addenbrooke's Hospital, Hills Road, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't