Search results for "Virus Replication"

showing 10 items of 199 documents

The Social Life of Viruses

2021

Despite their simplicity, viruses exhibit certain types of social interactions. Situations in which a given virus achieves higher fitness in combination with other members of the viral population have been described at the level of transmission, replication, suppression of host immune responses, and host killing, enabling the evolution of viral cooperation. Although cellular coinfection with multiple viral particles is the typical playground for these interactions, cooperation between viruses infecting different cells is also established through cellular and viral-encoded communication systems. In general, the stability of cooperation is compromised by cheater genotypes, as best exemplified…

genetic structuresGenotypeSpatial structurevirusesPopulationVirus-virus interactionsSuperinfection exclusionBiologyVirus ReplicationVirus03 medical and health sciencesVirologymedicineDefective interfering particleseducationViral evolution030304 developmental biology0303 health scienceseducation.field_of_studySocial evolution030306 microbiologyTransmission (medicine)Host (biology)Virionmedicine.diseaseCooperationEvolutionary biologyViral evolutionVirusesCoinfectionSocial evolutionAnnual Review of Virology
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Nuclear entry and egress of parvoviruses.

2022

Parvoviruses are small non-enveloped single-stranded DNA viruses, which depend on host cell nuclear transcriptional and replication machinery. After endosomal exposure of nuclear localization sequence and a phospholipase A2 domain on the capsid surface, and escape into the cytosol, parvovirus capsids enter the nucleus. Due to the small capsid diameter of 18–26 nm, intact capsids can potentially pass into the nucleus through nuclear pore complexes (NPCs). This might be facilitated by active nuclear import, but capsids may also follow an alternative entry pathway that includes activation of mitotic factors and local transient disruption of the nuclear envelope. The nuclear entry is followed b…

import and exportCell NucleusisäntäsolutviruksetparvovirusesNuclear Envelopenuclear pore complexesnucleusActive Transport Cell NucleusDNA Single-Strandednuclear envelopeVirus ReplicationMicrobiologyinfektiotParvovirusPhospholipasestumaNuclear PoreCapsid ProteinsMolecular BiologyparvoviruksetkapsidiMolecular microbiologyREFERENCES
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TLR7 controls VSV replication in CD169(+) SCS macrophages and associated viral neuroinvasion

2019

Vesicular stomatitis virus (VSV) is an insect-transmitted rhabdovirus that is neurovirulent in mice. Upon peripheral VSV infection, CD169+ subcapsular sinus (SCS) macrophages capture VSV in the lymph, support viral replication, and prevent CNS neuroinvasion. To date, the precise mechanisms controlling VSV infection in SCS macrophages remain incompletely understood. Here, we show that Toll-like receptor-7 (TLR7), the main sensing receptor for VSV, is central in controlling lymph-borne VSV infection. Following VSV skin infection, TLR7−/− mice display significantly less VSV titers in the draining lymph nodes (dLN) and viral replication is attenuated in SCS macrophages. In contrast to effects o…

lcsh:Immunologic diseases. Allergy0301 basic medicinevirusesImmunologyMedizinDENDRITIC CELLSRIG-IACTIVATION03 medical and health sciences0302 clinical medicinesubcapsular sinus macrophagesSUBCAPSULAR SINUS MACROPHAGESImmunitySIMULIUM-VITTATUM DIPTERAINFECTIONImmunology and Allergyinnate immunityvirus replicationHost factorconditional knock-out miceInnate immune systemScience & TechnologyLYMPH-NODESbiologysubcutaneous infectionPattern recognition receptorpattern recognition receptorsvirus diseasesTLR7VESICULAR STOMATITIS-VIRUSbiology.organism_classificationVirologyddc:Toll-like receptor 7stomatognathic diseases030104 developmental biologyViral replicationVesicular stomatitis virusNEW-JERSEY SEROTYPEINNATE IMMUNITYvesicular stomatitis viruslcsh:RC581-607Viral loadLife Sciences & Biomedicine030215 immunology
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Treatment of chronic hepatitis C

1991

alpha-Interferon given subcutaneously at doses between 1-3 million units leads to responses in about 50% of patients suffering from chronic hepatitis C. A 24-week treatment is frequently (approx. 50%) followed by relapses reducing the percentage of lasting responders to approx. 20%. The patients who relapse are sensitive to retreatment with interferon-alpha. A better understanding of HCV replication and of the interferon action in this viral disease might help to further improve treatment schedules. Side effects of interferon were frequently mild and readily reversible after cessation of treatment. At present interferon treatment should not be recommended in asymptomatic patients or individ…

medicine.medical_specialtyHepatologybusiness.industryTreatment outcomeInterferon-alphaHepacivirusVirus ReplicationProgressive liver diseaseHepatitis CAsymptomaticGastroenterologyTreatment OutcomeViral replicationChronic hepatitisInterferonInternal medicineChronic DiseaseImmunologyHumansMedicineViral diseaseMillion Unitsmedicine.symptombusinessmedicine.drugJournal of Hepatology
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Studies on a measles virus variant inducing persistent infections in cultured cells

1976

Attempts were made to characterized by a plaque assay two variants of the Edmonston strain of measles virus and to obtain plaque purified virus populations. The UP non-cytocidal variant, in all the examined cell systems, mainly produced small but also large plaques; the DP cytocidal variant always large plaques. Three clones, UP-SP4, UP-LP4 and DP-LP4, were derived by plaque purfication respectively of the UP small plaque, UP large plaque and DP large plaque forming particles. The virus populations of the clones could be distinguished by some other biological and physical characters: cytopathic effect in roller tube cultures, growth potential in HeLa cells, thermal stability at 45 degrees C…

medicine.medical_specialtyHot TemperaturevirusesViral Plaque AssayVirus Replicationcomplex mixturesVirusCell LineMeasles virusMedical microbiologyVirologyViral InterferencemedicineAnimalsCytopathic effectVirus quantificationStrain (chemistry)biologyDefective VirusesGenetic Variationvirus diseasesHaplorhiniGeneral MedicineIsolation (microbiology)biology.organism_classificationVirologyMeasles virusHeLa CellsArchives of Virology
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Neurotropism in newborn hamsters of plaque purified measles virus clones

1976

Three plaque purified measles virus clones displayed a different neurotropism in newborn hamsters.

medicine.medical_specialtyMesocricetusVirulencebiologyvirusesNeurotropismBrainGenetic VariationGeneral MedicineVirus Replicationbiology.organism_classificationVirologyCell LineMeasles virusMedical microbiologyAnimals NewbornCytopathogenic Effect ViralMeasles virusViral releaseInfectious disease (medical specialty)CricetinaeVirologymedicineAnimalsArchives of Virology
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Herpes simplex virus type 1 and 2 in the adrenal glands: Replication and histopathology

1986

The adrenal glands were shown to be the most severely infected organs in the early phase of HSV-1 infections (up to 10 days p.i.) after i.p. infections in mice. Virus could be isolated from the adrenal glands as early as one hour after infection with pathogenic and apathogenic strains. Infection of the adrenal glands is a result of viremia. The content of HSV-1 (5 strains) was much higher in the adrenals than in spleen and liver. It peaked at 3-4 days p.i. compared to 1-2 days in spleen and liver. Only strain 17 syn+ produced low tissue titres in the adrenal glands. Morphologic alterations by HSV-1 infections commenced with distinct foci 2 days after infection in the zona fasciculata, detec…

medicine.medical_specialtyRatónViremiaSpleenBiologyVirus Replicationmedicine.disease_causeHerpesviridaeVirusMiceVirologyAdrenal GlandsmedicineAnimalsSimplexvirusAntigens ViralAdrenal glandHerpes SimplexGeneral Medicinemedicine.diseaseVirologymedicine.anatomical_structureHerpes simplex virusLiverFemaleHistopathologySpleenArchives of Virology
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Rac1 and PAK1 are upstream of IKK-ε and TBK-1 in the viral activation of interferon regulatory factor-3

2004

The anti-viral type I interferon (IFN) response is initiated by the immediate induction of IFN beta, which is mainly controlled by the IFN-regulatory factor-3 (IRF-3). The signaling pathways mediating viral IRF-3 activation are only poorly defined. We show that the Rho GTPase Rac1 is activated upon virus infection and controls IRF-3 phosphorylation and activity. Inhibition of Rac1 leads to reduced IFN beta promoter activity and to enhanced virus production. As a downstream mediator of Rac signaling towards IRF-3, we have identified the kinase p21-activated kinase (PAK1). Furthermore, both Rac1 and PAK1 regulate the recently described IRF-3 activators, I kappa B kinase- and TANK-binding kina…

rac1 GTP-Binding ProteinTranscription GeneticBiophysicsIκB kinaseProtein Serine-Threonine KinasesSignal transductionBiologyVirus ReplicationBiochemistryCell LineDogsPAK1Structural BiologyInterferonGeneticsmedicineAnimalsHumansPhosphorylationPromoter Regions Geneticp21-activated kinasesMolecular BiologyRNA Double-StrandedKinaseRho GTPaseI-Kappa-B KinaseNuclear ProteinsInterferon-betaCell BiologyCREB-Binding ProteinI-kappa B KinaseDNA-Binding ProteinsEnzyme Activationp21-Activated KinasesInfluenza A virusViral infectionAnti-viral responseTrans-ActivatorsCancer researchInterferon Regulatory Factor-3Transcription factorSignal transductionDimerizationTranscription FactorsInterferon regulatory factorsmedicine.drugFEBS Letters
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Vaginal infection of mice with HSV type 2 variant ER−: A new animal model for human primary genital HSV type 2 infections

1992

Abstract Studying the pathogenesis of vaginal infections in mice with two variants of Herpes simplex virus type 2 (HSV-2) strain ER we observed that both variants ER+ and ER− caused severe vaginitis but only ER+ invaded the CNS leading to lethal neurological disease. In contrast, mice infected with ER− cleared the virus from the vagina and recovered from infection. ER+ and ER− expressed equal levels of thymidine kinase (TK) indicating a TK-independent difference in neurovirulence. Using the non-neurovirulent variant ER−, we were able to investigate humoral immune responses late after infection. Vaginal infection with ER− suppressed serum antibody formation after a secondary systemic HSV-1 i…

virusesBiologyVirus Replicationmedicine.disease_causeModels BiologicalVirusHerpesviridaePathogenesisMiceImmune systemVirologymedicineAnimalsSimplexvirusVaginitisMice Inbred BALB CHerpes GenitalisVirulencemedicine.diseaseVirologyMice Inbred C57BLDisease Models AnimalHerpes simplex virusmedicine.anatomical_structureAntibody FormationVaginaVaginabiology.proteinFemaleAntibodyJournal of Virological Methods
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Infection-induced chromatin modifications facilitate translocation of herpes simplex virus capsids to the inner nuclear membrane

2021

Herpes simplex virus capsids are assembled and packaged in the nucleus and move by diffusion through the nucleoplasm to the nuclear envelope for egress. Analyzing their motion provides conclusions not only on capsid transport but also on the properties of the nuclear environment during infection. We utilized live-cell imaging and single-particle tracking to characterize capsid motion relative to the host chromatin. The data indicate that as the chromatin was marginalized toward the nuclear envelope it presented a restrictive barrier to the capsids. However, later in infection this barrier became more permissive and the probability of capsids to enter the chromatin increased. Thus, although …

virusesGene ExpressionVirus ReplicationPathology and Laboratory Medicineherpes simplex -virusChlorocebus aethiopsCapsidsMedicine and Health SciencesSimplexvirusBiology (General)Mass DiffusivityStainingChromosome BiologyPhysicsChromatinChemistryMedical MicrobiologyViral PathogensPhysical SciencesVirusesHerpes Simplex Virus-1EpigeneticsCellular Structures and OrganellesPathogenskapsidiResearch ArticleHerpesvirusesNuclear EnvelopeQH301-705.5Biological Transport ActiveViral StructureResearch and Analysis MethodsinfektiotMicrobiologydiffuusio (fysikaaliset ilmiöt)CapsidNuclear MembraneVirologyGeneticsAnimalsherpesviruksetVero CellsMicrobial PathogensCell NucleusChemical PhysicsOrganismsBiology and Life SciencesHerpes SimplexCell Biologybiochemical phenomena metabolism and nutritionRC581-607Viral ReplicationHerpes Simplex VirusNuclear StainingSpecimen Preparation and TreatmentImmunologic diseases. AllergyDNA viruses
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