Search results for "REPLICATION"

showing 10 items of 489 documents

Replication of HSV-1 in murine peritoneal macrophages: comparison of various virus strains with different properties.

1984

The in vitro replication of eleven different strains of herpes simplex virus type 1 was studied in resident or thioglycollate-stimulated mouse macrophages. The strains of herpes simplex virus differed in the type of cytopathic effect, induction capacity for herpes simplex virus coded thymidine kinase and pathogenicity in the mouse. Herpes simplex virus replicated better in thioglycollate-stimulated macrophages than in resident macrophages. In vitro ageing of macrophages increased their replicative potency. Herpes simplex virus replicated better in macrophages from homozygous bg/bg C57/BL6J mice than in macrophages from their heterozygous littermates. Separation of macrophages on discontinuo…

ErythrocytesvirusesClone (cell biology)Mice Inbred StrainsBiologymedicine.disease_causeVirus ReplicationThymidine KinaseHerpesviridaeVirusMicrobiologychemistry.chemical_compoundMiceCytopathogenic Effect ViralPhagocytosisVirologymedicineMacrophageAnimalsAscitic FluidSimplexvirusCells CulturedCytopathic effectMacrophagesGeneral MedicineMacrophage ActivationVirologyMice Inbred C57BLHerpes simplex viruschemistryThymidine kinaseEnzyme InductionThymidineArchives of virology
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Why are viral genomes so fragile? The bottleneck hypothesis

2021

If they undergo new mutations at each replication cycle, why are RNA viral genomes so fragile, with most mutations being either strongly deleterious or lethal? Here we provide theoretical and numerical evidence for the hypothesis that genetic fragility is partly an evolutionary response to the multiple population bottlenecks experienced by viral populations at various stages of their life cycles. Modelling within-host viral populations as multi-type branching processes, we show that mutational fragility lowers the rate at which Muller’s ratchet clicks and increases the survival probability through multiple bottlenecks. In the context of a susceptible-exposed-infectious-recovered epidemiolog…

Evolutionary GeneticsRNA virusesMutation rateEpidemiologyExtinct GenomesMedicine and Health SciencesBiology (General)Genetics0303 health sciencesEvolutionary epidemiologyEcologyMicrobial MutationGenomicsDeletion MutationComputational Theory and MathematicsViral genomesGenetic EpidemiologyModeling and SimulationViral evolutionPopulation bottlenecksVirusesRNA ViralResearch ArticleQH301-705.5Genomics[SDV.CAN]Life Sciences [q-bio]/CancerContext (language use)Genome ViralBiologyMicrobiologyGenomic InstabilityViral EvolutionBottleneckEvolution Molecular03 medical and health sciencesCellular and Molecular NeuroscienceSurvival probabilityVirologyGeneticsFragilityMolecular BiologyEcology Evolution Behavior and Systematics030304 developmental biologyEvolutionary BiologyModels Genetic030306 microbiologyOrganismsComputational BiologyBiology and Life SciencesRNAVirus evolutionOrganismal EvolutionGenetic architecture[MATH.MATH-PR]Mathematics [math]/Probability [math.PR]Population bottleneckViral replicationMutationMicrobial Evolution
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Trapping the Enemy: Vermamoeba vermiformis Circumvents Faustovirus Mariensis Dissemination by Enclosing Viral Progeny inside Cysts

2019

Viruses depend on cells to replicate and can cause considerable damage to their hosts. However, hosts have developed a plethora of antiviral mechanisms to counterattack or prevent viral replication and to maintain homeostasis. Advantageous features are constantly being selected, affecting host-virus interactions and constituting a harsh race for supremacy in nature. Here, we describe a new antiviral mechanism unveiled by the interaction between a giant virus and its amoebal host. Faustovirus mariensis infects Vermamoeba vermiformis, a free-living amoeba, and induces cell lysis to disseminate into the environment. Once infected, the cells release a soluble factor that triggers the encystment…

Faustovirusfood.ingredientVermamoeba vermiformisviruksetantiviral mechanismsImmunologyamebatBiologyAntiviral mechanismMicrobiologyFaustovirusinfektiotVermamoeba vermiformisAmoeba (genus)03 medical and health sciencesfood[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseasesVirologyGiant Virus[SDV.MP.PAR]Life Sciences [q-bio]/Microbiology and Parasitology/ParasitologyamoebaComputingMilieux_MISCELLANEOUS030304 developmental biology0303 health sciences[SDV.MHEP.ME]Life Sciences [q-bio]/Human health and pathology/Emerging diseases030306 microbiologyVirology[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyOn cellsViral replicationInsect Science[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology
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Comparison of the genotoxic and apoptosis-inducing properties of ganciclovir and penciclovir in Chinese hamster ovary cells transfected with the thym…

2000

We studied the genotoxic and apoptosis-inducing properties of ganciclovir (GCV) and penciclovir (PCV) using Chinese hamster ovary cells stably transfected with the thymidine kinase (tk) gene of herpes simplex virus-1 (HSV-1). Cells expressing HSVtk were 300 and 100 times more sensitive than their isogenic HSVtk- counterparts to the cytotoxic effects of GCV and PCV, respectively. Using radiolabeled drugs, GCV was found to be incorporated into the genomic DNA much more effectively than PCV. GCV was highly potent in inducing chromosomal aberrations compared with PCV, which provoked less sister chromatid exchanges and chromosomal changes using equimolar or equitoxic doses. For both agents, apop…

GanciclovirDNA ReplicationCancer ResearchGuaninevirusesAcyclovirApoptosisCHO CellsHerpesvirus 1 HumanBiologymedicine.disease_causeTransfectioncomplex mixturesThymidine KinaseNecrosisCricetinaemedicineAnimalsMolecular BiologyGanciclovirMutagenicity TestsChinese hamster ovary cellCell CycleDNAGenetic TherapySuicide geneCell cycleMolecular biologyCell killingThymidine kinasePenciclovirMolecular MedicineSister Chromatid ExchangeGenotoxicitymedicine.drugCancer gene therapy
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Enhancerless Cytomegalovirus Is Capable of Establishing a Low-Level Maintenance Infection in Severely Immunodeficient Host Tissues but Fails in Expon…

2010

ABSTRACT Major immediate-early transcriptional enhancers are genetic control elements that act, through docking with host transcription factors, as a decisive regulatory unit for efficient initiation of the productive virus cycle. Animal models are required for studying the function of enhancers paradigmatically in host organs. Here, we have sought to quantitatively assess the establishment, maintenance, and level of in vivo growth of enhancerless mutants of murine cytomegalovirus in comparison with those of an enhancer-bearing counterpart in models of the immunocompromised or immunologically immature host. Evidence is presented showing that enhancerless viruses are capable of forming restr…

Gene Expression Regulation ViralMutantImmunology/dk/atira/pure/subjectarea/asjc/2400/2406CytomegalovirusMice SCIDBiologyMicrobiologyVirusImmunocompromised HostMiceExponential growthIn vivoVirologyAnimalsHumans/dk/atira/pure/subjectarea/asjc/2400/2403EnhancerTranscription factorMice Inbred BALB CVirologyGenome Replication and Regulation of Viral Gene ExpressionEnhancer Elements GeneticInsect ScienceCytomegalovirus InfectionsHost-Pathogen InteractionsCytomegalovirus infections
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Patchwork Pattern of Transcriptional Reactivation in the Lungs Indicates Sequential Checkpoints in the Transition from Murine Cytomegalovirus Latency…

1999

The lungs are a relevant organ site of primary and recurrent human cytomegalovirus (hCMV) disease (for overviews, see references 21, 22, 31, 34, 39, and 44). Murine CMV (mCMV) can serve us as a model for studying CMV pneumonia in acute infection (6, 27, 33, 37) as well as for studying viral latency, reactivation, and recurrence in the lungs (2, 17, 18, 42, 43). We have shown recently that transcription from the major immediate-early (MIE) transcription unit ie1-ie3 (hereafter referred to as ie1/3), which is driven by a strong MIE promoter-enhancer (MIEPE) (3), occurs during pulmonary latency of mCMV but fails to initiate the productive cycle (17). Notably, the paralogous MIEPE of hCMV can f…

Gene Expression Regulation ViralTranscriptional ActivationHuman cytomegalovirusvirusesImmunologyCytomegalovirusReplicationBiologyMicrobiologyMiceTransactivationTranscription (biology)VirologyGene expressionVirus latencymedicineAnimalsEnhancerGenes Immediate-EarlyLungTranscription factorMice Inbred BALB CEffectormedicine.diseaseVirologyVirus LatencyInsect ScienceCytomegalovirus InfectionsFemaleVirus ActivationTranscription FactorsJournal of Virology
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Dealing with the Pseudo-Replication Problem in Longitudinal Data from Posidonia Oceanica Surveys: Modeling Dependence vs. Subsampling

2012

Posidonia oceanica represents the key species of the most important ecosystem in subtidal habitats of the Mediterranean Sea. Being sensitive to changes in the environment, it is considered a crucial indicator of the quality of coastal marine waters. A peculiarity of P. oceanica is the presence of reiterative modules characterizing its growth, which lend themselves to back-dating techniques, allowing for the reconstruction of past history of growth variables (annual rhizome elongation and diameter, primary production, etc.). Such back-dating techniques provide, for each sampled shoot, a longitudinal series of multivariate data; this is an instance of what Hurlbert (1984) in a seminal paper d…

Generalized linear mixed modelSub-samplingPseudo-replicationMarine ecolology
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Reply to Côté and Willer: New replication attempts provide no evidence that inequality moderates the effect of income on generosity

2020

Cote et al. (1) provided evidence that economic inequality moderates the effect of income on generosity. In their study, individuals with higher household income were less generous in a dictator game than poorer individuals only if they resided in a US state with comparatively large economic inequality. We questioned this finding because we did not find any evidence for the postulated moderation effect of economic inequality across three studies (ref. 2; for similar replication failures see ref. 3). However, our studies were conceptual rather than direct replications as we used different measures of generosity (charitable donations, behavior in a trust game, and volunteering) and also inclu…

GenerosityMultidisciplinaryInequalitymedia_common.quotation_subject05 social sciencesModeration050105 experimental psychologyReplication (computing)03 medical and health sciences0302 clinical medicineDictator gameEconomic inequalityState (polity)EconomicsHousehold income0501 psychology and cognitive sciencesDemographic economics030217 neurology & neurosurgerymedia_commonProceedings of the National Academy of Sciences
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Dominant-negative FADD rescues the in vivo fitness of a cytomegalovirus lacking an anti-apoptotic viral gene

2008

ABSTRACT Genes that inhibit apoptosis have been described for many DNA viruses. Herpesviruses often contain even more than one gene to control cell death. Apoptosis inhibition by viral genes is postulated to contribute to viral fitness, although a formal proof is pending. To address this question, we studied the mouse cytomegalovirus (MCMV) protein M36, which binds to caspase-8 and blocks death receptor-induced apoptosis. The growth of MCMV recombinants lacking M36 (ΔM36) was attenuated in vitro and in vivo. In vitro, caspase inhibition by zVAD-fmk blocked apoptosis in ΔM36-infected macrophages and rescued the growth of the mutant. In vivo, ΔM36 infection foci in liver tissue contained sign…

Genes ViralFas-Associated Death Domain ProteinvirusesImmunologyMutantCytomegalovirusCellular Response to InfectionApoptosisMicrobiologyVirusCell LineMiceIn vivoVirologyAnimalsFADDCaspaseDNA PrimersGenes DominantMice Inbred BALB CBase Sequencebiologyanti-apoptotic viral geneBIOMEDICINE AND HEALTHCARE. Basic Medical Sciences.MCMV; FADD; anti-apoptotic viral geneFlow CytometryMolecular biologyMice Inbred C57BLViral replicationApoptosisVirion assemblyInsect ScienceFADDbiology.proteinBIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti.MCMV
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Chasing the Origin of Viruses: Capsid-Forming Genes as a Life-Saving Preadaptation within a Community of Early Replicators

2015

Virus capsids mediate the transfer of viral genetic information from one cell to another, thus the origin of the first viruses arguably coincides with the origin of the viral capsid. Capsid genes are evolutionarily ancient and their emergence potentially predated even the origin of first free-living cells. But does the origin of the capsid coincide with the origin of viruses, or is it possible that capsid-like functionalities emerged before the appearance of true viral entities? We set to investigate this question by using a computational simulator comprising primitive replicators and replication parasites within a compartment matrix. We observe that systems with no horizontal gene transfer…

Genes ViralSciencevirusesorigin of virusesBiologyVirus Physiological PhenomenaVirus ReplicationEvolution Molecularvirus capsids03 medical and health sciencesCompartment (development)Gene030304 developmental biologyGenetics0303 health sciencesMultidisciplinaryModels Genetic030306 microbiologyHuman evolutionary geneticsta1184ta1183QRBiological Evolutioncapsid genesCapsidViral replicationViral evolutionHorizontal gene transferMedicineCapsid ProteinsResearch ArticleVirus Physiological Phenomena
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