| pubmed-article:16476701 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16476701 | lifeskim:mentions | umls-concept:C0220847 | lld:lifeskim |
| pubmed-article:16476701 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:16476701 | lifeskim:mentions | umls-concept:C0023820 | lld:lifeskim |
| pubmed-article:16476701 | lifeskim:mentions | umls-concept:C0074129 | lld:lifeskim |
| pubmed-article:16476701 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
| pubmed-article:16476701 | lifeskim:mentions | umls-concept:C1413218 | lld:lifeskim |
| pubmed-article:16476701 | lifeskim:mentions | umls-concept:C0205296 | lld:lifeskim |
| pubmed-article:16476701 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
| pubmed-article:16476701 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:16476701 | pubmed:dateCreated | 2006-4-3 | lld:pubmed |
| pubmed-article:16476701 | pubmed:abstractText | The possible role of candidate receptors in the cellular penetration of HCV from serum of infected patients remains unclear. SR-BI/Cla1 interacts with plasma HDL, native and modified LDL, and VLDL, and facilitates cellular cholesterol efflux to lipoprotein acceptors. SR-BI/Cla1 binds HCV E2 protein and interacts with HCV pseudotypes via the HVR1 of the E2 envelope glycoprotein. Our data reveal that functional SR-BI/Cla1 expressed on the surface of CHO cells mediates the binding and uptake of HCV from the sera of infected patients. Interaction between HCV and SR-BI/Cla1 is not sensitive to either anti-E2 or anti-HVR1 antibodies but is effectively inhibited by anti-betalipoprotein antibodies and competed out by apoB-containing lipoproteins and notably by VLDL. We interpret our data to indicate that VLDL associated with or incorporated into HCV plays a critical role in the primary interaction of HCV with SR-BI/Cla1, whereas the HCV E2 protein does not. In addition, our findings in hepatoma cell lines suggest that the interaction of HCV with human hepatocytes is equally mediated, at least in a part, by VLDL, and as such may represent an alternative pathway for infection. The association of HCV with ApoB-containing lipoproteins may promote cellular uptake of this virus in the presence of neutralizing antibodies. | lld:pubmed |
| pubmed-article:16476701 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16476701 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16476701 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16476701 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16476701 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16476701 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16476701 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16476701 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:16476701 | pubmed:issn | 1530-6860 | lld:pubmed |
| pubmed-article:16476701 | pubmed:author | pubmed-author:ChapmanJohnJ | lld:pubmed |
| pubmed-article:16476701 | pubmed:author | pubmed-author:HubyThierryT | lld:pubmed |
| pubmed-article:16476701 | pubmed:author | pubmed-author:MaillardPatri... | lld:pubmed |
| pubmed-article:16476701 | pubmed:author | pubmed-author:BudkowskaAgat... | lld:pubmed |
| pubmed-article:16476701 | pubmed:author | pubmed-author:MoreauMartine... | lld:pubmed |
| pubmed-article:16476701 | pubmed:author | pubmed-author:AndréoUrsulaU | lld:pubmed |
| pubmed-article:16476701 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:16476701 | pubmed:volume | 20 | lld:pubmed |
| pubmed-article:16476701 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16476701 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16476701 | pubmed:pagination | 735-7 | lld:pubmed |
| pubmed-article:16476701 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:16476701 | pubmed:meshHeading | pubmed-meshheading:16476701... | lld:pubmed |
| pubmed-article:16476701 | pubmed:meshHeading | pubmed-meshheading:16476701... | lld:pubmed |
| pubmed-article:16476701 | pubmed:meshHeading | pubmed-meshheading:16476701... | lld:pubmed |
| pubmed-article:16476701 | pubmed:meshHeading | pubmed-meshheading:16476701... | lld:pubmed |
| pubmed-article:16476701 | pubmed:meshHeading | pubmed-meshheading:16476701... | lld:pubmed |
| pubmed-article:16476701 | pubmed:meshHeading | pubmed-meshheading:16476701... | lld:pubmed |
| pubmed-article:16476701 | pubmed:meshHeading | pubmed-meshheading:16476701... | lld:pubmed |
| pubmed-article:16476701 | pubmed:meshHeading | pubmed-meshheading:16476701... | lld:pubmed |
| pubmed-article:16476701 | pubmed:meshHeading | pubmed-meshheading:16476701... | lld:pubmed |
| pubmed-article:16476701 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16476701 | pubmed:articleTitle | The interaction of natural hepatitis C virus with human scavenger receptor SR-BI/Cla1 is mediated by ApoB-containing lipoproteins. | lld:pubmed |
| pubmed-article:16476701 | pubmed:affiliation | Hepacivirus Unit, Pasteur Institute, Paris, France. | lld:pubmed |
| pubmed-article:16476701 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16476701 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:949 | entrezgene:pubmed | pubmed-article:16476701 | lld:entrezgene |
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