<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>81(11)</volume><submitter>Rodrigue-Gervais IG</submitter><pubmed_abstract>The role of peripheral dendritic cells (DCs) in hepatitis C virus (HCV) infection is unclear. To determine if persistent infection exerts an inhibitory pressure on HCV-specific innate responses, we analyzed DC function in blood through quantification of cell-associated HCV RNA levels in conjunction with multiparametric flow cytometry analysis of pathogen recognition receptor-induced cytokine expression. Independently of the serum viral load, fluorescence-activated cell sorter-purified total DCs had a wide range of cell-associated HCV genomic RNA copy numbers (mean log(10), 5.0 per 10(6) cells; range, 4.3 to 5.8). Here we report that for viremic patients with high viral loads in their total DCs, the myeloid DC (MDC) subset displayed impaired expression of interleukin-12 (IL-12) and tumor ne</pubmed_abstract><journal>Journal of virology</journal><pagination>5537-46</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC1900294</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Poly(I:C) and lipopolysaccharide innate sensing functions of circulating human myeloid dendritic cells are affected in vivo in hepatitis C virus-infected patients.</pubmed_title><pmcid>PMC1900294</pmcid><pubmed_authors>Willems B</pubmed_authors><pubmed_authors>Rodrigue-Gervais IG</pubmed_authors><pubmed_authors>Sauve D</pubmed_authors><pubmed_authors>Sekaly RP</pubmed_authors><pubmed_authors>Beaule G</pubmed_authors><pubmed_authors>Jouan L</pubmed_authors><pubmed_authors>Lamarre D</pubmed_authors><pubmed_authors>Bruneau J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Poly(I:C) and lipopolysaccharide innate sensing functions of circulating human myeloid dendritic cells are affected in vivo in hepatitis C virus-infected patients.</name><description>The role of peripheral dendritic cells (DCs) in hepatitis C virus (HCV) infection is unclear. To determine if persistent infection exerts an inhibitory pressure on HCV-specific innate responses, we analyzed DC function in blood through quantification of cell-associated HCV RNA levels in conjunction with multiparametric flow cytometry analysis of pathogen recognition receptor-induced cytokine expression. Independently of the serum viral load, fluorescence-activated cell sorter-purified total DCs had a wide range of cell-associated HCV genomic RNA copy numbers (mean log(10), 5.0 per 10(6) cells; range, 4.3 to 5.8). Here we report that for viremic patients with high viral loads in their total DCs, the myeloid DC (MDC) subset displayed impaired expression of interleukin-12 (IL-12) and tumor ne</description><dates><release>2007-01-01T00:00:00Z</release><publication>2007 Jun</publication><modification>2025-04-03T22:51:51.068Z</modification><creation>2019-03-27T02:04:15Z</creation></dates><accession>S-EPMC1900294</accession><cross_references><pubmed>17376921</pubmed><doi>10.1128/jvi.01741-06</doi><doi>10.1128/JVI.01741-06</doi></cross_references></HashMap>