Search results for "Virus Replication"

showing 10 items of 199 documents

Clonal Interference and the Evolution of RNA Viruses

1999

In asexual populations, beneficial mutations that occur in different lineages compete with one another. This phenomenon, known as clonal interference, ensures that those beneficial mutations that do achieve fixation are of large effect. Clonal interference also increases the time between fixations, thereby slowing the adaptation of asexual populations. The effects of clonal interference were measured in the asexual RNA virus vesicular stomatitis virus; rates and average effects of beneficial mutations were quantified.

GeneticsLikelihood FunctionsModels StatisticalMultidisciplinaryGenes ViralbiologyClonal interferenceRNARNA virusVirus Replicationbiology.organism_classificationAdaptation PhysiologicalBiological EvolutionModels BiologicalVesicular stomatitis Indiana virusCell LineGene FrequencyVesicular stomatitis virusCricetinaeMutationConfidence IntervalsAnimalsScience
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Prisoner's dilemma in an RNA virus

1999

The evolution of competitive interactions among viruses1 was studied in the RNA phage φ6 at high and low multiplicities of infection (that is, at high and low ratios of infecting phage to host cells). At high multiplicities, many phage infect and reproduce in the same host cell, whereas at low multiplicities the viruses reproduce mainly as clones. An unexpected result of this study1 was that phage grown at high rates of co-infection increased in fitness initially, but then evolved lowered fitness. Here we show that the fitness of the high-multiplicity phage relative to their ancestors generates a pay-off matrix conforming to the prisoner's dilemma strategy of game theory2,3. In this strateg…

GeneticsMultidisciplinarybiologyvirusesmedia_common.quotation_subjectRNARNA virusPrisoner's dilemmaVirus Replicationbiology.organism_classificationBiological EvolutionModels BiologicalVirusCystovirusBacteriophage phi 6BacteriophageGame TheoryMutationMicrobial cooperationSelfishnessmedia_commonNature
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The cost of replication fidelity in an RNA virus

2005

It is often argued that high mutation rates are advantageous for RNA viruses, because they confer elevated rates of adaptation. However, there is no direct evidence showing a positive correlation between mutation and adaptation rates among RNA viruses. Moreover, theoretical work does not argue in favor of this prediction. We used a series of vesicular stomatitis virus clones harboring single amino acid substitutions in the RNA polymerase to demonstrate that changes inducing enhanced fidelity paid a fitness cost, but that there was no positive correlation between mutation an adaptation rates. We demonstrate that the observed mutation rate in vesicular stomatitis virus can be explained by a t…

GeneticsMutation rateMultidisciplinaryAdaptation BiologicalRNARNA virusDNA-Directed RNA PolymerasesBiological SciencesBiologyVesicular stomatitis Indiana virusVirus Replicationbiology.organism_classificationVirologyVesicular stomatitis Indiana viruschemistry.chemical_compoundAmino Acid SubstitutionchemistryViral replicationVesicular stomatitis virusRNA polymeraseMutation (genetic algorithm)Mutagenesis Site-DirectedSelection GeneticProceedings of the National Academy of Sciences
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The sf32 unique gene of Spodoptera frugiperda multiple nucleopolyhedrovirus (SfMNPV) is a non-essential gene that could be involved in nucleocapsid o…

2013

A recombinant virus lacking the sf32 gene (Sf32null), unique to the Spodoptera frugiperda multiple nucleopolyhedrovirus (SfMNPV), was generated by homologous recombination from a bacmid comprising the complete viral genome (Sfbac). Transcriptional analysis revealed that sf32 is an early gene. Occlusion bodies (OBs) of Sf32null contained 62% more genomic DNA than viruses containing the sf32 gene, Sfbac and Sf32null-repair, although Sf32null DNA was three-fold less infective when injected in vivo. Sf32null OBs were 18% larger in diameter and contained 17% more nucleocapsids within ODVs than those of Sfbac. No significant differences were detected in OB pathogenicity (50% lethal concentration)…

GenotypevirusesScienceGenome ViralSpodopteraSpodopteraVirus ReplicationOcclusion-derived virionsRecombinant virusHomology (biology)VirusViral Proteins03 medical and health sciencesAnimalsNucleocapsidSpodoptera frugiperda multiple nucleopolyhedrovirus (SfMNPV)Gene030304 developmental biology0303 health sciencesGenes Essential[SDV.BA.MVSA]Life Sciences [q-bio]/Animal biology/Veterinary medicine and animal HealthMultidisciplinaryNucleocapsid organizationbiology030306 microbiologyfungiQVirionRbiology.organism_classificationVirologyNucleopolyhedroviruses3. Good healthViral replicationEssential geneLarvaDNA Viral[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/VirologyMedicinesf32Homologous recombinationResearch ArticlePLoS ONE
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Translation of hepatitis B virus (HBV) surface proteins from the HBV pregenome and precore RNAs in Semliki Forest virus-driven expression.

2004

Hepatitis B virus (HBV) pregenome RNA (pgRNA) serves as a translation template for the HBV core (HBc) protein and viral polymerase (Pol). HBV precore RNA (pcRNA) directs the synthesis of the precore (preC) protein, a precursor of the hepatitis B e antigen (HBeAg). pgRNA and pcRNA were expressed in the Semliki Forest virus (SFV) expression system. Besides the HBc and preC proteins, there was revealed the synthesis of all three forms of HBV surface (HBs) proteins: long (LHBs), middle (MHBs) and short (SHBs), the start codons of which are located more than 1000 nt downstream of the HBc and preC start codons. Moreover, other HBV templates, such as 3′-truncated pgRNA lacking 3′ direct repeat and…

HBV RNA encapsidation signal epsilonHepatitis B virusvirusesGene ExpressionLeaky scanningDNA-Directed DNA Polymerasemedicine.disease_causeSemliki Forest virusVirus ReplicationCell LineViral Envelope ProteinsVirologymedicineAnimalsHepatitis B e AntigensRNA MessengerCloning MolecularProtein PrecursorsHepatitis B virusHepatitis B Surface Antigensbiologyvirus diseasesRNA virusTemplates Geneticbiology.organism_classificationVirologyMolecular biologyHepatitis B Core AntigensImmunohistochemistrySemliki forest virusdigestive system diseasesGenetic translationHBeAgHepadnaviridaeProtein BiosynthesisRNA ViralThe Journal of general virology
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Mutations in DNA Binding and Transactivation Domains Affect the Dynamics of Parvovirus NS1 Protein

2013

ABSTRACT The multifunctional replication protein of autonomous parvoviruses, NS1, is vital for viral genome replication and for the control of viral protein production. Two DNA-interacting domains of NS1, the N-terminal and helicase domains, are necessary for these functions. In addition, the N and C termini of NS1 are required for activation of viral promoter P38. By comparison with the structural and biochemical data from other parvoviruses, we identified potential DNA-interacting amino acid residues from canine parvovirus NS1. The role of the identified amino acids in NS1 binding dynamics was studied by mutagenesis, fluorescence recovery after photobleaching, and computer simulations. Mu…

HMG-boxParvovirus CaninevirusesImmunologyDNA Mutational AnalysisMutation MissenseNS1 proteiiniViral Nonstructural ProteinsVirus ReplicationMicrobiologyNS1 proteinSingle-stranded binding proteinCell LineSeqA protein domainVirologyAnimalsDNA bindingReplication protein AbiologyTer proteinparvovirusvirus diseasesDNAn sitoutuminen [DNA]biochemical phenomena metabolism and nutritionMolecular biologyCell biologyVirus-Cell InteractionsProtein Structure TertiaryDNA binding siteDNA-Binding ProteinsInsect Sciencebiology.proteinMutant ProteinsViral genome replicationBinding domainProtein Binding
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Immune activation promotes evolutionary conservation of T-cell epitopes in HIV-1.

2013

The immune system should constitute a strong selective pressure promoting viral genetic diversity and evolution. However, HIV shows lower sequence variability at T-cell epitopes than elsewhere in the genome, in contrast with other human RNA viruses. Here, we propose that epitope conservation is a consequence of the particular interactions established between HIV and the immune system. On one hand, epitope recognition triggers an anti-HIV response mediated by cytotoxic T-lymphocytes (CTLs), but on the other hand, activation of CD4(+) helper T lymphocytes (TH cells) promotes HIV replication. Mathematical modeling of these opposite selective forces revealed that selection at the intrapatient l…

Helper T lymphocyteQH301-705.5HIV AntigensEpitopes T-LymphocyteHIV InfectionsImmunodominanceBiologyVirus ReplicationGeneral Biochemistry Genetics and Molecular BiologyEpitopeEvolution Molecular03 medical and health sciencesImmune systemCytotoxic T cellHumansComputer SimulationAmino Acid SequenceBiology (General)BiologyConserved Sequence030304 developmental biologyImmune Evasion0303 health sciencesImmunity CellularGeneral Immunology and MicrobiologyModels Genetic030306 microbiologyGeneral NeuroscienceGenetic VariationViral LoadVirology3. Good healthEpitope mappingHIV AntigensViral replicationImmunologyHost-Pathogen InteractionsSynopsisHIV-1General Agricultural and Biological SciencesAlgorithms
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Hepatitis B protein HBx binds the DLEU2 lncRNA to sustain cccDNA and host cancer-related gene transcription.

2019

Objective: The HBV HBx regulatory protein is required for transcription from the covalently closed circular DNA (cccDNA) minichromosome and affects the epigenetic control of both viral and host cellular chromatin. Design: We explored, in relevant cellular models of HBV replication, the functional consequences of HBx interaction with DLEU2, a long non-coding RNA (lncRNA) expressed in the liver and increased in human hepatocellular carcinoma (HCC), in the regulation of host target genes and the HBV cccDNA. Results: We show that HBx binds the promoter region, enhances the transcription and induces the accumulation of DLEU2 in infected hepatocytes. We found that nuclear DLEU2 directly binds HBx…

Hepatitis B virusCarcinoma Hepatocellular2312HepatologyvirusesLiver NeoplasmsCell Culture Techniquesmacromolecular substanceshepatocellular carcinomaVirus Replicationliverdigestive system diseasesHepatocytesTrans-ActivatorsHumansEnhancer of Zeste Homolog 2 ProteinRNA Long NoncodingViral Regulatory and Accessory Proteins1506hepatitis BDNA CircularGut
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Overexpression of STAT-1 by adenoviral gene transfer does not inhibit hepatitis B virus replication.

2006

Objectives Interferons are known to inhibit the replication of hepatitis B viruses (HBV) in several animal models in vitro and in vivo as well in humans. The STAT-1 protein plays a central role in the biological activity of both type I and type II interferons. The lack of functional STAT-1 renders cells and organisms susceptible to bacterial and viral infectious agents. We analysed whether the overexpression of STAT-1 protein enhances the biological interferon response and whether it elicits antiviral acitivity against HBV in vitro. Methods To achieve an efficient STAT-1 overexpression in primary liver cells and hepatoma cells, we generated a recombinant, replication-deficient adenovirus ex…

Hepatitis B virusCarcinoma HepatocellularBlotting WesternGenetic Vectorsmedicine.disease_causeTransfectionVirus ReplicationVirusHepatitis B virus PRE betaAdenoviridaeOrthohepadnavirusInterferonmedicineTumor Cells CulturedAnimalsHumansCells CulturedHepatitis B virusHepatologybiologyLiver NeoplasmsGastroenterologyvirus diseasesHepatitis Bmedicine.diseasebiology.organism_classificationVirologyMolecular biologydigestive system diseasesIn vitroDucksSTAT1 Transcription FactorHepadnaviridaeGene Expression RegulationDNA ViralHepatocytesmedicine.drugEuropean journal of gastroenterologyhepatology
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Virus replication and virion export in X-deficient hepatitis B virus transgenic mice

2002

The function of the X protein (pX) in the replication cycle of mammalian hepadnaviruses is enigmatic. Using tissue culture experiments it has been shown that the X gene product is not central to hepatitis B virus (HBV) replication and virion export. However, at present it is still unclear whether this also applies to the in vivo situation. Using a terminally redundant X-deficient HBV DNA construct, transgenic mice were established that exhibited high-level expression of the viral core protein in liver and kidneys. Importantly, replicative DNA intermediates and mature viral genomes could be detected in the liver and serum of these mice, respectively. These findings indicate that, in the in v…

Hepatitis B virusHepatitis B virus DNA polymerasevirusesTransgeneMice TransgenicBiologyVirus Replicationmedicine.disease_causeHepatitis B virus PRE betaGene productMicechemistry.chemical_compoundVirologymedicineAnimalsViral Regulatory and Accessory ProteinsHepatitis B virusVirionVirologyMolecular biologydigestive system diseasesMice Inbred C57BLHBxViral replicationchemistryMice Inbred DBATrans-ActivatorsDNAJournal of General Virology
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