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Journal Article
PLoS ONE, ISSN 1932-6203, 07/2015, Volume 10, Issue 7, p. e0133236
Serum levels of the interferon (IFN)-stimulated chemokine CXCL10 are increased during chronic HCV infection and associate with outcome of IFN-based therapy.... 
VIRUS-INFECTION | CHEMOKINES | MULTIDISCIPLINARY SCIENCES | CHRONIC HEPATITIS-C | PROTEIN-10 | GENOTYPE 1 INFECTION | PREDICTIVE-VALUE | RIBAVIRIN | INDUCTION | ASSOCIATION | SPONTANEOUS CLEARANCE | Recurrence | Interferons | Humans | Fluorenes - therapeutic use | Dipeptidyl Peptidase 4 - blood | Hepatitis C, Chronic - virology | Male | Adult | Female | Hepacivirus - physiology | Drug Therapy, Combination | Benzimidazoles - therapeutic use | Hepacivirus - drug effects | Sofosbuvir - therapeutic use | Virus Replication - drug effects | Chemokine CXCL10 - blood | Antiviral Agents - therapeutic use | Ribavirin - therapeutic use | Dipeptidyl Peptidase 4 - genetics | Treatment Outcome | Hepatitis C, Chronic - drug therapy | Hepatitis C, Chronic - blood | Convalescence | Chemokine CXCL10 - genetics | Protein Processing, Post-Translational | Hepatitis C, Chronic - genetics | Viral Load - drug effects | Infection | Care and treatment | Analysis | Interferon | Biological response modifiers | Hepatitis C virus | Health aspects | Therapy | Laboratories | Chronic infection | Critical care | Amino acids | Infections | Ribavirin | Clinical outcomes | Proteins | Genotype & phenotype | Hepatitis | Immunology | Hepatology | Post-translation | Pretreatment | Drug dosages | Genotypes | Statistical analysis | Liver diseases | Dendritic cells | Serum levels | Studies | Infectious diseases | CXCL10 protein | Biomarkers | Chemokines | Virus Replication/drug effects | Viral Load/drug effects | Dipeptidyl Peptidase 4/blood | Dipeptidyl Peptidase 4/genetics | Chemokine CXCL10/blood | Hepatitis C, Chronic/blood | Life Sciences | Hepatitis C, Chronic/drug therapy | Hepatitis C, Chronic/virology | Hepatitis C, Chronic/genetics | Chemokine CXCL10/genetics | Benzimidazoles/therapeutic use | Hepacivirus/physiology | Fluorenes/therapeutic use | Antiviral Agents/therapeutic use | Sofosbuvir/therapeutic use | Hepacivirus/drug effects | Ribavirin/therapeutic use
Journal Article
Journal Article
Nature medicine, ISSN 1546-170X, 2011, Volume 17, Issue 5, pp. 589 - 595
Hepatitis C virus (HCV) is a major cause of liver disease, but therapeutic options are limited and there are no prevention strategies. Viral entry is the first... 
MEDICINE, RESEARCH & EXPERIMENTAL | ACTIVATION | B TYPE-I | NEUTRALIZING ANTIBODIES | BIOCHEMISTRY & MOLECULAR BIOLOGY | MOUSE | FACTOR RECEPTOR | CELL BIOLOGY | EPIDERMAL-GROWTH-FACTOR | CELL TRANSMISSION | HUMAN LIVER | INFECTION | ERLOTINIB | Erlotinib Hydrochloride | RNA, Small Interfering - genetics | Receptor, Epidermal Growth Factor - genetics | Hepatitis C - therapy | Humans | Virus Internalization - drug effects | RNA Interference | Membrane Proteins - physiology | Base Sequence | Hepacivirus - physiology | Hepatitis C - prevention & control | Receptor, Epidermal Growth Factor - physiology | Hepacivirus - drug effects | Cell Line | Antiviral Agents - pharmacology | Receptor, EphA2 - physiology | Tetraspanin 28 | Claudin-1 | Animals | Hepatitis C - virology | Receptor, EphA2 - genetics | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Antigens, CD - physiology | Hepatitis C - physiopathology | Ligands | Mice | Protein Kinase Inhibitors - pharmacology | Receptor, EphA2 - antagonists & inhibitors | Quinazolines - pharmacology | Host-Pathogen Interactions - physiology | Ephrin A | Antiviral agents | Care and treatment | Patient outcomes | Physiological aspects | Research | Hepatitis C | Hepatitis | Viruses | Drug therapy | Antiviral drugs | Receptor, EphA2 | Hépatology and Gastroenterology | Antigens, CD81 | Antiviral Agents | Quinazolines | Virus Internalization | Membrane Proteins | Host-Pathogen Interactions | Life Sciences | Human health and pathology | Protein Kinase Inhibitors | RNA, Small Interfering | Hepacivirus | Antigens, CD | Receptor, Epidermal Growth Factor | Liver | HCV escape variants | Cell-cell transmission | genetics | pharmacology | Antiviral | therapy | physiology | drug effects | prevention & control | antagonists & inhibitors | physiopathology | Phosphotyrosine kinase | virology
Journal Article
Gastroenterology, ISSN 0016-5085, 2014, Volume 146, Issue 5, pp. 1373 - 1385.e11
Background & Aims Positive-sense RNA viruses remodel intracellular membranes to generate specialized membrane compartments for viral replication. Several RNA... 
Gastroenterology and Hepatology | Viral Replication | Phosphatidylinositol 4-Phosphate | Lipid Kinase | Lipid Transfer Proteins | Keywords | COMPLEX | ACTIVATION | 4-Phosphate | RNA REPLICATION | LIPID RAFT | Phosphatidylinositol | IN-VITRO | HEPATITIS-C VIRUS | III ALPHA | CELL-CULTURE | INFECTION | GASTROENTEROLOGY & HEPATOLOGY | Phosphatidylinositol Phosphates - metabolism | Receptors, Steroid - metabolism | Humans | Hepacivirus - genetics | Hepacivirus - pathogenicity | Viral Proteins - metabolism | 1-Phosphatidylinositol 4-Kinase - metabolism | Transfection | Biological Transport | RNA Interference | HEK293 Cells | Cell Membrane - drug effects | Hepacivirus - drug effects | Virus Replication - drug effects | RNA, Viral - biosynthesis | Viral Proteins - genetics | 1-Phosphatidylinositol 4-Kinase - antagonists & inhibitors | Genotype | Cholesterol - metabolism | Host-Pathogen Interactions | Cell Membrane - enzymology | Hepacivirus - enzymology | Phenotype | Receptors, Steroid - genetics | Hepacivirus - growth & development | Viral Nonstructural Proteins - metabolism | Protein Kinase Inhibitors - pharmacology | HeLa Cells | RNA | Phospholipids | Hepatitis C virus | Hepatitis C | Phosphotransferases | Cholesterol | Protein binding | viral replication | lipid transfer proteins | lipid kinase | phosphatidylinositol 4-phosphate
Journal Article
Gastroenterology, ISSN 0016-5085, 2010, Volume 139, Issue 3, pp. 953 - 964.e4
Background & Aims Hepatitis C virus (HCV) infection is a challenge to prevent and treat because of the rapid development of drug resistance and escape. Viral... 
Gastroenterology and Hepatology | Genetic Barrier | Antiviral | Treatment | Receptor | Host Factor | B TYPE-I | LIVER-TRANSPLANTATION | SOURCE OUTBREAK | ESCAPE | PROTECT | RESPONSES | BROADLY NEUTRALIZING ANTIBODIES | GASTROENTEROLOGY & HEPATOLOGY | BINDING | VIRAL ENTRY | Antibodies, Monoclonal - toxicity | Antibody Specificity | Cricetulus | Antiviral Agents - toxicity | Humans | Hepacivirus - genetics | Hepacivirus - pathogenicity | Antiviral Agents - metabolism | Virus Internalization - drug effects | Dose-Response Relationship, Drug | Hepatitis C - immunology | Hepatitis C - prevention & control | Hepatocytes - drug effects | CHO Cells | Binding, Competitive | Hepacivirus - drug effects | Cell Survival - drug effects | Antiviral Agents - pharmacology | Cricetinae | Antibodies, Monoclonal - pharmacology | Genotype | Membrane Proteins - immunology | Epitopes | Hepatocytes - immunology | Claudin-1 | Hep G2 Cells | Animals | Membrane Proteins - antagonists & inhibitors | Hepatocytes - virology | Antibodies, Monoclonal - metabolism | Binding Sites, Antibody | Prevention | Antiviral agents | Disease transmission | Gastrointestinal agents | Immunoglobulin G | Fluorescence | Monoclonal antibodies | Drug resistance | Hepatitis C | Hepatitis C virus | Health aspects | Infection control | Hépatology and Gastroenterology | Cell Survival | Antiviral Agents | Antibodies, Monoclonal | Virus Internalization | Membrane Proteins | Life Sciences | Human health and pathology | Hepatocytes | Hepacivirus
Journal Article
Journal of Virology, ISSN 0022-538X, 2017, Volume 91, Issue 1
Journal Article