Search results for "NS2-3 protease"

showing 10 items of 11 documents

Stop codon insertion restores the particle formation ability of hepatitis B virus core-hantavirus nucleocapsid protein fusions.

2003

In recent years, epitopes of various origin have been inserted into the core protein of hepatitis B virus (HBc), allowing the formation of chimeric HBc particles. Although the C-terminus of a C-terminally truncated HBc (HBcΔ) tolerates the insertion of extended foreign sequences, the insertion capacity is still a limiting factor for the construction of multivalent vaccines. Previously, we described a new system to generate HBcΔ mosaic particles based on a read-through mechanism in an <i>Escherichia coli</i> suppressor strain [J Gen Virol 1997;78:2049–2053]. Those mosaic particles allowed the insertion of a 114-amino acid (aa)-long segment of a Puumala hantavirus (PUUV) nucleocap…

Hepatitis B virusHepatitis B virus DNA polymerasevirusesRecombinant Fusion ProteinsMolecular Sequence Datamedicine.disease_causeEpitopeHepatitis B virus PRE betaMiceVirologyparasitic diseasesmedicineAnimalsNucleocapsidHantavirusHepatitis B virusMice Inbred BALB CBase SequenceChemistryHepatitis B virus coreVirionvirus diseasesNucleocapsid ProteinsVirologyMolecular biologyHepatitis B Core Antigensdigestive system diseasesStop codonNS2-3 proteaseInfectious DiseasesCodon TerminatorImmunizationIntervirology
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Characterization of cell lines carrying self-replicating hepatitis C virus RNAs.

2001

ABSTRACT Subgenomic selectable RNAs of the hepatitis C virus (HCV) have recently been shown to self-replicate to high levels in the human hepatoma cell line Huh-7 (V. Lohmann, F. Körner, J. O. Koch, U. Herian, L. Theilmann, and R. Bartenschlager, Science 285:110–113, 1999). Taking advantage of this cell culture system that allows analyses of the interplay between HCV replication and the host cell, in this study we characterized two replicon-harboring cell lines that have been cultivated for more than 1 year. During this time, we observed no signs of cytopathogenicity such as reduction of growth rates or ultrastructural changes. High levels of HCV RNAs were preserved in cells passaged under…

Hepatitis C virusImmunoelectron microscopyImmunologyHepacivirusBiologyViral Nonstructural Proteinsmedicine.disease_causeVirus ReplicationMicrobiologyViral ProteinsVirologymedicineTumor Cells CulturedHumansRepliconPhosphorylationNS5ARNAVirologyMolecular biologyVirus-Cell InteractionsNS2-3 proteaseViral replicationCell cultureInsect ScienceRNA ViralRepliconJournal of virology
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Replication of subgenomic hepatitis C virus RNAs in a hepatoma cell line.

1999

An estimated 170 million persons worldwide are infected with hepatitis C virus (HCV), a major cause of chronic liver disease. Despite increasing knowledge of genome structure and individual viral proteins, studies on virus replication and pathogenesis have been hampered by the lack of reliable and efficient cell culture systems. A full-length consensus genome was cloned from viral RNA isolated from an infected human liver and used to construct subgenomic selectable replicons. Upon transfection into a human hepatoma cell line, these RNAs were found to replicate to high levels, permitting metabolic radiolabeling of viral RNA and proteins. This work defines the structure of HCV replicons funct…

Carcinoma HepatocellularVirus CultivationvirusesHepatitis C virusDrug ResistanceGenome ViralHepacivirusBiologyViral Nonstructural Proteinsmedicine.disease_causeTransfectionVirus ReplicationViruschemistry.chemical_compoundmedicineTumor Cells CulturedHumansCloning MolecularNS5ANS5BSubgenomic mRNAGeneticsNS3MultidisciplinaryLiver NeoplasmsVirologyHepatitis CNS2-3 proteaseViral replicationchemistryRNA ViralRepliconGentamicinsScience (New York, N.Y.)
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Biochemical and structural analysis of the NS5B RNA-dependent RNA polymerase of the hepatitis C virus.

2000

Hepatitis C virus (HCV), the major causative agent of chronic and sporadic non-A, non-B hepatitis worldwide, is a distinct member of the Flaviviridae virus family. These viruses have in common a plus-strand RNA genome that is replicated in the cytoplasm of the infected cell via minus-strand RNA intermediates. Owing to the lack of reliable cell culture systems and convenient animal models for HCV, the mechanisms governing RNA replication are not known. As a first step towards the development of appropriate in vitro systems, we expressed the NS5B RNA-dependent RNA polymerase (RdRp) in insect cells, purified the protein to near homogeneity and studied its biochemical properties. It is a primer…

virusesHepatitis C virusGenetic VectorsRNA-dependent RNA polymeraseHepacivirusViral Nonstructural Proteinsmedicine.disease_causeCell LineSubstrate Specificitychemistry.chemical_compoundTranscription (biology)Sequence Analysis ProteinVirologyRNA polymeraseRibavirinmedicineHumansNS5BPolymeraseHepatologybiologyRNANucleosidesDNA-Directed RNA PolymerasesRNA-Dependent RNA PolymeraseVirologyRecombinant ProteinsNS2-3 proteaseInfectious DiseaseschemistryMutationbiology.proteinRNABaculoviridaeJournal of viral hepatitis
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Sequences in the 5′ Nontranslated Region of Hepatitis C Virus Required for RNA Replication

2001

ABSTRACT Sequences in the 5′ and 3′ termini of plus-strand RNA viruses harbor cis -acting elements important for efficient translation and replication. In case of the hepatitis C virus (HCV), a plus-strand RNA virus of the family Flaviviridae , a 341-nucleotide-long nontranslated region (NTR) is located at the 5′ end of the genome. This sequence contains an internal ribosome entry site (IRES) that is located downstream of an about 40-nucleotide-long sequence of unknown function. By using our recently developed HCV replicon system, we mapped and characterized the sequences in the 5′ NTR required for RNA replication. We show that deletions introduced into the 5′ terminal 40 nucleotides abolis…

Hepatitis C virusImmunologyRNA-dependent RNA polymeraseReplicationHepacivirusmedicine.disease_causeOrigin of replicationMicrobiologyVirologymedicineTumor Cells CulturedHumansRepliconGeneticsbiologyRNARNA virusbiology.organism_classificationVirologyNS2-3 proteaseInternal ribosome entry siteInsect ScienceProtein BiosynthesisRNA ViralReplicon5' Untranslated Regions
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Persistent and Transient Replication of Full-Length Hepatitis C Virus Genomes in Cell Culture

2002

ABSTRACT The recently developed subgenomic hepatitis C virus (HCV) replicons were limited by the fact that the sequence encoding the structural proteins was missing. Therefore, important information about a possible influence of these proteins on replication and pathogenesis and about the mechanism of virus formation could not be obtained. Taking advantage of three cell culture-adaptive mutations that enhance RNA replication synergistically, we generated selectable full-length HCV genomes that amplify to high levels in the human hepatoma cell line Huh-7 and can be stably propagated for more than 6 months. The structural proteins are efficiently expressed, with the viral glycoproteins E1 and…

ImmunologyReplicationGenome ViralHepacivirusBiologyVirus ReplicationMicrobiologyVirusViral ProteinsGene FrequencyVirologyTumor Cells CulturedHumansSubgenomic mRNAchemistry.chemical_classificationEndoplasmic reticulumRNAHepatitis CMolecular biologyNS2-3 proteasechemistryViral replicationCell cultureCulture Media ConditionedInsect ScienceRNA ViralGlycoproteinSubcellular FractionsJournal of Virology
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Interferon-γ inhibits replication of subgenomic and genomic hepatitis C virus RNAs

2002

Persistent infection with hepatitis C virus (HCV) is a major cause of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. All treatments known so far rely on the antiviral activity of interferon alfa (IFN-alpha) that is given alone or in combination with ribavirin. Unfortunately, only a fraction of the patients clear the virus during therapy and for those who do not respond there is currently no alternative treatment. Selectable subgenomic HCV RNAs (replicons) have been recently used to investigate the effect of IFN-alpha on HCV replication. However, it has not yet been analyzed whether other cytokines also play a role in the innate immune response against HCV. Here we show th…

HepatologyHepatitis C virusvirus diseasesBiologymedicine.disease_causeVirologydigestive system diseasesVirusNS2-3 proteaseCell killingViral replicationmedicineInterferon gammaInterferon alfamedicine.drugSubgenomic mRNAHepatology
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Interferon-alpha inhibits hepatitis C virus subgenomic RNA replication by an MxA-independent pathway.

2001

Hepatitis C virus (HCV) persists in the majority of infected individuals and is a major cause of chronic hepatitis, liver cirrhosis and hepatocellular carcinoma. Chronic hepatitis C is currently treated with interferon (IFN)-α or with a combination of IFN-α and ribavirin. The availability of an HCV replicon system (Lohmann et al., Science 285, 110–113, 1999) allowed the investigation of the effects of IFN on genuine HCV replication in cultured cells. It is shown here that IFN-α inhibits subgenomic HCV RNA replication in HuH-7 human hepatoma cells. Immunofluorescence, Western blot and Northern blot analysis revealed that levels of both HCV protein and replicon RNA were reduced after treatme…

Myxovirus Resistance ProteinsHepatitis C virusHepacivirusBiologyViral Nonstructural Proteinsmedicine.disease_causeAntiviral Agentschemistry.chemical_compoundInterferonGTP-Binding ProteinsVirologymedicineTumor Cells CulturedHumansRepliconNorthern blotSubgenomic mRNADose-Response Relationship DrugRibavirinvirus diseasesRNAInterferon-alphaProteinsVirologyMolecular biologydigestive system diseasesNS2-3 proteasechemistryRNA ViralRepliconmedicine.drugThe Journal of general virology
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Complex formation between the NS3 serine-type proteinase of the hepatitis C virus and NS4A and its importance for polyprotein maturation

1995

Processing of the hepatitis C virus polyprotein is mediated by host cell signalases and at least two virally encoded proteinases. Of these, the serine-type proteinase encompassing the amino-terminal one-third of NS3 is responsible for cleavage at the four sites carboxy terminal of NS3. The activity of this proteinase is modulated by NS4A, a 54-amino-acid polyprotein cleavage product essential for processing at the NS3/4A, NS4A/4B, and NS4B/5A sites and enhancing cleavage efficiency between NS5A and NS5B. Using the vaccinia virus-T7 hybrid system to express hepatitis C virus polypeptides in BHK-21 cells, we studied the role of NS4A in proteinase activation. We found that the NS3 proteinase a…

Protein ConformationRecombinant Fusion ProteinsvirusesGenetic VectorsMolecular Sequence DataImmunologyVaccinia virusHepacivirusProtein Sorting SignalsViral Nonstructural ProteinsBiologyKidneyTransfectionCleavage (embryo)MicrobiologyAntibodiesCell LineSerineEpitopesViral Proteinschemistry.chemical_compoundProtein structureProteinase 3CricetinaeVirologyAnimalsAmino Acid SequenceProtein PrecursorsNS5BPeptide sequenceNS3Sequence Homology Amino AcidSerine Endopeptidasesvirus diseasesbiochemical phenomena metabolism and nutritiondigestive system diseasesNS2-3 proteaseBiochemistrychemistryInsect ScienceProtein Processing Post-TranslationalAlgorithmsRNA HelicasesResearch ArticleJournal of Virology
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The NS3/4A proteinase of the hepatitis C virus: unravelling structure and function of an unusual enzyme and a prime target for antiviral therapy

1999

The hepatitis C virus (HCV) is a major causative agent of transfusion-acquired and sporadic non-A, non-B hepatitis worldwide. Infections most often persist and lead, in approximately 50% of all patients, to chronic liver disease. As is characteristic for a member of the family Flaviviridae, HCV has a plus-strand RNA genome encoding a polyprotein, which is cleaved co- and post-translationally into at least 10 different products. These cleavages are mediated, among others, by a virally encoded chymotrypsin-like serine proteinase located in the N-terminal domain of non-structural protein 3 (NS3). Activity of this enzyme requires NS4A, a 54-residue polyprotein cleavage product, to form a stable…

Models MolecularProtein ConformationvirusesHepatitis C virusMolecular Sequence DataHepacivirusViral Nonstructural ProteinsBiologymedicine.disease_causeAntiviral AgentsSerineProtein structureVirologymedicineProtease InhibitorsAmino Acid SequenceHepatitischemistry.chemical_classificationNS3HepatologySerine EndopeptidasesRNAmedicine.diseaseVirologyNS2-3 proteaseInfectious DiseasesEnzymechemistryRNA HelicasesJournal of Viral Hepatitis
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