Search results for "HEPATITIS"

showing 10 items of 1578 documents

APOBEC3-mediated restriction of RNA virus replication

2018

AbstractAPOBEC3 family members are cytidine deaminases with roles in intrinsic responses to infection by retroviruses and retrotransposons, and in the control of other DNA viruses, such as herpesviruses, parvoviruses and hepatitis B virus. Although effects of APOBEC3 members on viral DNA have been demonstrated, it is not known whether they edit RNA genomes through cytidine deamination. Here, we investigated APOBEC3-mediated restriction of Coronaviridae. In experiments in vitro, three human APOBEC3 proteins (A3C, A3F and A3H) inhibited HCoV-NL63 infection and limited production of progeny virus, but did not cause hypermutation of the coronaviral genome. APOBEC3-mediated restriction was parti…

0301 basic medicineHepatitis B virusviruseslcsh:MedicineGenome Viralmedicine.disease_causeVirus ReplicationVirusArticleCell LineCytosine Deaminase03 medical and health scienceschemistry.chemical_compoundCytidine deaminationCytidine DeaminasemedicineCoronaviridaeHumansRNA VirusesAPOBEC Deaminaseslcsh:ScienceCoronavirusMultidisciplinarybiology630 Agriculturelcsh:RDNA VirusesRNARNA virusbiochemical phenomena metabolism and nutritionbiology.organism_classificationVirology3. Good health030104 developmental biologyNucleoproteinschemistryViral replicationRNA570 Life sciences; biologylcsh:QDNA
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Failure on voxilaprevir, velpatasvir, sofosbuvir and efficacy of rescue therapy

2021

Background & Aims There are limited data on patients with chronic HCV infection in whom combination voxilaprevir (VOX), velpatasvir (VEL), sofosbuvir (SOF) retreatment fails. Thus, we aimed to assess treatment failure and rescue treatment options in these patients. Methods Samples from 40 patients with HCV genotypes (GT) 1-4 in whom VOX/VEL/SOF retreatment failed were collected within the European Resistance Study Group. Population-based resistance analyses were conducted and clinical parameters and retreatment efficacies were evaluated retrospectively in 22 patients. Results Most VOX/VEL/SOF failure patients were infected with HCV GT3a (n = 18, 45%) or GT1a (n = 11, 28%) and had cirrhosis …

0301 basic medicineHepatitis C Virusmedicine.medical_specialtySofosbuvirVoxilaprevirPopulationresistance-associated substitutionsDirect-acting antiviralVoxilaprevir/velpatasvir/sofosbuvir.GastroenterologySettore MED/07Telaprevir03 medical and health scienceschemistry.chemical_compound0302 clinical medicineVoxilaprevir/Velpatasvir/SofosbuvirInternal medicineBoceprevirRescue therapymedicineResistance-associated substitutioneducationdirect-acting antiviralsDAAeducation.field_of_studyHepatologybusiness.industryvirus diseasesGlecaprevirDAA; HCV; Hepatitis C Virus; Voxilaprevir/Velpatasvir/Sofosbuvir; direct-acting antivirals; rescue therapy; resistance-associated substitutionsdigestive system diseasesPibrentasvirRegimen030104 developmental biologychemistryHCV030211 gastroenterology & hepatologyHepatitis C virubusinessmedicine.drugJournal of Hepatology
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Molecular targets in inhibition of hepatitis C virus replication

1997

Hepatitis C virus (HCV) is the major cause of transfusion-associated hepatitis and accounts for a significant proportion of hepatitis cases worldwide. Most, if not all, infections become persistent and about 60% of cases develop chronic liver disease with various outcomes ranging from an asymptomatic carrier state to chronic active hepatitis and liver cirrhosis, which is strongly associated with the development of hepatocellular carcinoma. Since the initial cloning of the viral genome in 1989, our knowledge of the molecular biology of HCV has increased rapidly and led to the identification of several potential targets for antiviral intervention. In contrast, the low replication of the virus…

0301 basic medicineHepatitisCirrhosisbiologyHepatitis C virus030106 microbiologyGeneral Medicinebiology.organism_classificationmedicine.diseaseChronic liver diseasemedicine.disease_cause01 natural sciencesVirologyVirus0104 chemical sciences010404 medicinal & biomolecular chemistry03 medical and health sciencesFlaviviridaeDrug developmentHepatocellular carcinomaImmunologymedicine
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Interferon lambda 4 rs368234815 TT>δG variant is associated with liver damage in patients with nonalcoholic fatty liver disease

2017

Background and Aims: The IFNL3/4 locus influencing innate immunity regulation has been associated with the severity of hepatitis and fibrosis progression during chronic hepatitis C infection, while contrasting results were reported in NAFLD. In this study, we examined whether rs12979860 and the linked causal rs368234815 variant encoding for the alternative IFNL4 protein variant are associated with liver fibrosis and damage in a large multicenter cohort of patients at risk of NASH. To clarify the mechanism, we also evaluated the impact on interferon-stimulated gene (ISG) hepatic expression in a subset of patients. Methods: We considered 946 consecutive Italian individuals at risk of NASH wit…

0301 basic medicineHepatitismedicine.medical_specialtyNAFLD NASH IFNL4Hepatologybusiness.industryLocus (genetics)medicine.diseaseGastroenterology03 medical and health sciences030104 developmental biology0302 clinical medicineFibrosisInternal medicineNonalcoholic fatty liver diseaseCohortGenotypemedicine030211 gastroenterology & hepatologyAllelebusinessProspective cohort studyHepatology
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Clinical significance of detectable and quantifiable HCV RNA at the end of treatment with ledipasvir/sofosbuvir in GT1 patients

2018

Background & aims AASLD/IDSA treatment guidelines for hepatitis C virus (HCV) infection state that testing for quantitative HCV RNA can be considered at the end of antiviral treatment (EOT) with interferon-free regimens. However, it remains unclear how to respond to a detectable or even quantifiable HCV RNA result. The aim of this study was to analyse the frequency and predictive value of detectable and quantifiable HCV RNA results at the EOT in patients with HCV genotype 1 infection treated with ledipasvir (LDV) and sofosbuvir (SOF) ± ribavirin (RBV) in a large real-world cohort. Methods A retrospective analysis of the DHC-R (Deutsches Hepatitis C-Register, German Hepatitis C-Registry) coh…

0301 basic medicineLedipasvirMalemedicine.medical_specialtySofosbuvirSustained Virologic ResponseHepatitis C virusMedizinHepacivirusmedicine.disease_causeGastroenterologyAntiviral Agents03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineGermanyRibavirinMedicineHumansClinical significanceRegistriesRetrospective StudiesHepatitisFluorenesHepatologybusiness.industryRibavirinvirus diseasesHepatitis CViral Loadmedicine.diseaseHepatitis Cdigestive system diseases030104 developmental biologychemistryRNA Viral030211 gastroenterology & hepatologyBenzimidazolesFemaleSofosbuvirbusinessUridine MonophosphateViral loadmedicine.drug
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Association between Leptin and Complement in Hepatitis C Patients with Viral Clearance: Homeostasis of Metabolism and Immunity

2016

Background The association between leptin and complement in hepatitis C virus (HCV) infection remains unknown. Methods A prospective study was conducted including 474 (250 genotype 1, 224 genotype 2) consecutive chronic hepatitis C (CHC) patients who had completed an anti-HCV therapy course and undergone pre-therapy and 24-week post-therapy assessments of interferon λ3-rs12979860 and HCV RNA/genotypes, anthropometric measurements, metabolic and liver profiles, and complement component 3 (C3), C4, and leptin levels. Results Of the 474 patients, 395 had a sustained virological response (SVR). Pre-therapy leptin levels did not differ between patients with and without an SVR. Univariate and mul…

0301 basic medicineLeptinRNA virusesMaleSteatosisSustained Virologic ResponsePhysiologyPeptide Hormoneslcsh:MedicineAminotransferasesHepacivirusmedicine.disease_causeGastroenterologyBiochemistryBody Mass IndexCytopathologychemistry.chemical_compoundMathematical and Statistical TechniquesHomeostasisProspective Studieslcsh:SciencePathology and laboratory medicineMultidisciplinaryComplement component 3Hepatitis C virusLeptinAlanine TransaminaseComplement C4Hepatitis CComplement C3Medical microbiologyMiddle AgedLipidsEnzymesmedicine.anatomical_structureCholesterolVirusesPhysical SciencesRNA ViralFemaleViral ClearancePathogensStatistics (Mathematics)Research ArticleAdultmedicine.medical_specialtyGenotypeHepatitis C virusResearch and Analysis MethodsMicrobiologyAntiviral AgentsPolymorphism Single Nucleotide03 medical and health sciencesTransferasesWhite blood cellInternal medicineVirologymedicineHumansStatistical MethodsAgedMedicine and health sciencesFlavivirusesCholesterolbusiness.industryInterleukinslcsh:ROrganismsViral pathogensBiology and Life SciencesProteinsComplement System ProteinsHepatitis C Chronicmedicine.diseaseHormonesHepatitis virusesMicrobial pathogens030104 developmental biologychemistryAnatomical PathologyImmunologyMultivariate AnalysisEnzymologylcsh:QInterferonsSteatosisbusinessPhysiological ProcessesBody mass indexMathematicsViral Transmission and InfectionPLoS ONE
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Determinants of fibrosis progression and regression in NASH

2017

Cirrhosis has become the major liver-related clinical endpoint in non-alcoholic steatohepatitis (NASH). However, progression to cirrhosis is less predictable in NASH than in other chronic liver diseases. This is due to the complex and multifactorial aetiology of NASH, which is determined by lifestyle and nutrition, multiple genetic and epigenetic factors, and a prominent role of hepatic and extrahepatic comorbidities. Thus, modest changes in these cofactors can also induce fibrosis regression, at least in patients with precirrhotic liver disease. Fibrogenesis in NASH correlates with, but is indirectly coupled to, classical inflammation, since fibrosis progression is driven by repetitive per…

0301 basic medicineLiver CirrhosisCirrhosisInflammationBioinformaticsCholangiocyte03 medical and health sciencesLiver disease0302 clinical medicineFibrosisNon-alcoholic Fatty Liver DiseaseClinical endpointMedicineHumansHepatologybusiness.industryDisease Managementmedicine.diseasePrognosis3. Good health030104 developmental biologyImmunologyHepatic stellate cellDisease Progression030211 gastroenterology & hepatologySteatohepatitismedicine.symptombusinessJournal of Hepatology
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Transcriptomic profiling across the nonalcoholic fatty liver disease spectrum reveals gene signatures for steatohepatitis and fibrosis

2020

International audience; The mechanisms that drive nonalcoholic fatty liver disease (NAFLD) remain incompletely understood. This large multicenter study characterized the transcriptional changes that occur in liver tissue across the NAFLD spectrum as disease progresses to cirrhosis to identify potential circulating markers. We performed high-throughput RNA sequencing on a discovery cohort comprising histologically characterized NAFLD samples from 206 patients. Unsupervised clustering stratified NAFLD on the basis of disease activity and fibrosis stage with differences in age, aspartate aminotransferase (AST), type 2 diabetes mellitus, and carriage of PNPLA3 rs738409 , a genetic variant assoc…

0301 basic medicineLiver CirrhosisCirrhosis[SDV]Life Sciences [q-bio]DiseaseBiologyTranscriptome03 medical and health sciences0302 clinical medicineFibrosisnashNon-alcoholic Fatty Liver DiseaseDiabetes mellitusNonalcoholic fatty liver diseasemedicineDiabetes MellitusHumansGeneral Medicinemedicine.disease3. Good health030104 developmental biologyDiabetes Mellitus Type 2LiverHumans; Liver; Liver Cirrhosis; Transcriptome; Diabetes Mellitus Type 2; Non-alcoholic Fatty Liver DiseaseImmunology030211 gastroenterology & hepatologyGDF15SteatohepatitisTranscriptomeType 2
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Hepatocyte pyroptosis and release of inflammasome particles induce stellate cell activation and liver fibrosis.

2019

Background & Aims Increased hepatocyte death contributes to the pathology of acute and chronic liver diseases. However, the role of hepatocyte pyroptosis and extracellular inflammasome release in liver disease is unknown. Methods We used primary mouse and human hepatocytes, hepatocyte-specific leucine 351 to proline Nlrp3KICreA mice, and GsdmdKO mice to investigate pyroptotic cell death in hepatocytes and its impact on liver inflammation and damage. Extracellular NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasomes were isolated from mutant NLRP3-YFP HEK cells and internalisation was studied in LX2 and primary human hepatic stellate cells. We also examined a cohort of 154…

0301 basic medicineLiver CirrhosisInflammasomesInterleukin-1betaArticle03 medical and health sciencesLiver diseaseMice0302 clinical medicineMice Inbred NODNon-alcoholic Fatty Liver DiseaseNLR Family Pyrin Domain-Containing 3 ProteinmedicineHepatic Stellate CellsPyroptosisAnimalsHumansLiver injuryHepatologyChemistryFatty liverCaspase 1PyroptosisInflammasomemedicine.disease3. Good healthCell biology030104 developmental biologymedicine.anatomical_structureHepatocyteHepatic stellate cellHepatocytesProtein Translocation Systems030211 gastroenterology & hepatologySteatohepatitisReactive Oxygen Speciesmedicine.drugJournal of hepatology
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Nuclear Translocation of RELB Is Increased in Diseased Human Liver and Promotes Ductular Reaction and Biliary Fibrosis in Mice.

2019

Background & Aims Cholangiocyte proliferation and ductular reaction contribute to the onset and progression of liver diseases. Little is known about the role of the transcription factor nuclear factor-κB (NF-κB) in this process. We investigated the activities of the RELB proto-oncogene NF-κB subunit in human cholangiocytes and in mouse models of liver disease characterized by a ductular reaction. Methods We obtained liver tissue samples from patients with primary sclerosing cholangitis, primary biliary cholangitis, hepatitis B or C virus infection, autoimmune hepatitis, alcoholic liver disease, or without these diseases (controls) from a tissue bank in Germany. Tissues were analyzed by immu…

0301 basic medicineLiver CirrhosisMaleAlcoholic liver diseaseCholangiocyte proliferationAutoimmune hepatitisProto-Oncogene MasLiver diseaseMice0302 clinical medicineCarbon TetrachlorideCells CulturedRELBLiver DiseasesGastroenterologyMiddle Aged3. Good healthDeubiquitinating Enzyme CYLDCysteine EndopeptidasesProtein TransportLiverGene Knockdown TechniquesCytokines030211 gastroenterology & hepatologyFemaleCell activationAdultLymphotoxin-betaAdolescentCholangitis SclerosingPrimary sclerosing cholangitis03 medical and health sciencesYoung AdultLymphotoxin beta ReceptormedicineAnimalsHumansRNA MessengerParenchymal TissueAgedCell ProliferationCell NucleusHepatologybusiness.industryTranscription Factor RelBEpithelial CellsDicarbethoxydihydrocollidinemedicine.diseaseFibrosis030104 developmental biologyCancer researchLiver functionBile DuctsbusinessGastroenterology
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