Linked Life Data

16729312

Source:http://linkedlifedata.com/resource/pubmed/id/16729312

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2006-5-31
pubmed:abstractText
Initiation of hepatitis C virus (HCV) infection is mediated by docking of the viral envelope to the hepatocyte cell surface membrane followed by entry of the virus into the host cell. Aiming to elucidate the impact of this interaction on host cell biology, we performed a genomic analysis of the host cell response following binding of HCV to cell surface proteins. As ligands for HCV-host cell surface interaction, we used recombinant envelope glycoproteins and HCV-like particles (HCV-LPs) recently shown to bind or enter hepatocytes and human hepatoma cells. Gene expression profiling of HepG2 hepatoma cells following binding of E1/E2, HCV-LPs, and liver tissue samples from HCV-infected individuals was performed using a 7.5-kd human cDNA microarray. Cellular binding of HCV-LPs to hepatoma cells resulted in differential expression of 565 out of 7,419 host cell genes. Examination of transcriptional changes revealed a broad and complex transcriptional program induced by ligand binding to target cells. Expression of several genes important for innate immune responses and lipid metabolism was significantly modulated by ligand-cell surface interaction. To assess the functional relevance and biological significance of these findings for viral infection in vivo, transcriptional changes were compared with gene expression profiles in liver tissue samples from HCV-infected patients or controls. Side-by-side analysis revealed that the expression of 27 genes was similarly altered following HCV-LP binding in hepatoma cells and viral infection in vivo. In conclusion, HCV binding results in a cascade of intracellular signals modulating target gene expression and contributing to host cell responses in vivo. Reprogramming of cellular gene expression induced by HCV-cell surface interaction may be part of the viral strategy to condition viral entry and replication and escape from innate host cell responses.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0270-9139
pubmed:author
pubmed:issnType
Print
pubmed:volume
43
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1326-36
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16729312-Antigens, Viral, pubmed-meshheading:16729312-Base Sequence, pubmed-meshheading:16729312-Carrier Proteins, pubmed-meshheading:16729312-Cell Line, Tumor, pubmed-meshheading:16729312-Cells, Cultured, pubmed-meshheading:16729312-Gene Expression Regulation, pubmed-meshheading:16729312-Hepacivirus, pubmed-meshheading:16729312-Hepatitis C, pubmed-meshheading:16729312-Host Cell Factor C1, pubmed-meshheading:16729312-Humans, pubmed-meshheading:16729312-Molecular Sequence Data, pubmed-meshheading:16729312-Protein Array Analysis, pubmed-meshheading:16729312-RNA, Viral, pubmed-meshheading:16729312-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:16729312-Sensitivity and Specificity, pubmed-meshheading:16729312-Tissue Culture Techniques, pubmed-meshheading:16729312-Viral Envelope Proteins
pubmed:year
2006
pubmed:articleTitle
Host cell responses induced by hepatitis C virus binding.
pubmed:affiliation
Department of Medicine II, University of Freiburg, Freiburg, Germany.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't