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Microtubules and microfilaments in HSV-Infected rabbit-kidney cells.

1981

In rabbit kidney cells infected with strains of Herpes simplex virus producing either cell-rounding or polycaryocytosis. Vinblastine induced paracrystals. This could be shown by phase-contrast- and electron-microscopy. Infections were done under one-step-growth conditions or at low MOI. 90 per cent noninfected cells contained stress fibers as detected by Servablue R250-staining. Shortly after recruitment into polycaryocytes, stress fibres of normal length appearing in criss-cross arrangement can be seen in the periphery of these cells. Later they polymerize to very long fibers and finally they are partially destroyed. The time of destruction depends on the MOI employed. By using Actinomycin…

virusesBiologyCycloheximideMicrofilamentmedicine.disease_causeKidneyVinblastineMicrotubulesCell LineCell Fusionchemistry.chemical_compoundViral ProteinsCytopathogenic Effect ViralVirologymedicineAnimalsSimplexvirusCytoskeletonKidneyCell fusionGeneral MedicineVirologyVinblastinemedicine.anatomical_structureHerpes simplex viruschemistryGiant cellCell cultureDNA ViralRabbitsmedicine.drugArchives of virology
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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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Replication of herpes simplex virus type 1 and 2 in the medulla of the adrenal gland after vaginal infection of mice.

1996

After vaginal infections of mice with neuroinvasive strains of herpes simplex virus type 1 and 2 (HSV-1, HSV-2) virus replicates in the epithelium of the vagina, in the paravaginal ganglia, in the spinal cord and finally in the brain and in the adrenal glands. However, viral antigens could be demonstrated only in the medulla of the adrenal glands but not in the cortex, as assessed by immunohistochemistry (IHC). HSV could not be isolated from liver, spleen, uterus, and ovaries. This contrasts to the intraperitoneal (i.p) route of infection with replication in different visceral organs including the adrenal gland's cortex.

virusesHerpesvirus 2 HumanUterusSpleenHerpesvirus 1 HumanBiologymedicine.disease_causeVirus ReplicationHerpesviridaeVirusMiceVirologyChlorocebus aethiopsmedicineAnimalsHumansAntigens ViralVero CellsMedullaCerebral CortexMice Inbred BALB CAdrenal glandGeneral MedicineVirologymedicine.anatomical_structureHerpes simplex virusSpinal CordAdrenal MedullaVaginaVaginaFemaleArchives of virology
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Translocation of the nuclear autoantigen La to the cell surface of herpes simplex virus type 1 infected cells.

1992

Recently we developed a procedure to translocalize one of the extractable nuclear antigens (ENAs), the La protein, to the cell surface of CV-1 cells. Here we report that herpes simplex virus type 1 infection can also induce a translocation of the autoantigen to the cell surface. On the cell surface we detected La protein assembled with large protrusions. Within these protrusions La protein colocalized with virus particles. These protrusions are known to be released from the cell after virus infections. Such complexes consisting of self and virus could provide helper determinants for an anti-self response, and therefore be important in generation of autoimmunity.

virusesImmunologyCellmedicine.disease_causeAutoantigensVirusHerpesviridaeSingle-stranded binding proteinAntigenAlphaherpesvirinaeCricetinaemedicineImmunology and AllergyAnimalsNuclear proteinCells CulturedCell NucleusbiologyAntibodies MonoclonalBiological TransportHerpes Simplexbiology.organism_classificationBlood Physiological PhenomenaVirologymedicine.anatomical_structureHerpes simplex virusRibonucleoproteinsbiology.proteinAutoimmunity
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The human autoantigen La/SS-B accelerates herpes simplex virus type 1 replication in transfected mouse 3T3 cells.

1998

SUMMARY Permanently transfected mouse cell lines which expressed different levels of the human autoantigen La/SS-B were infected with different strains of herpes simplex virus type 1, including the strains ANG, HSZP, 17syn+ and HFEM. During infection the localization of the human La protein was followed using an anti-La MoAb, which recognized only the human La protein but did not cross-react with either the endogenous mouse La protein or any viral encoded protein. After infection La protein was transported from the nucleus to the cytoplasm. The time course of translocation was dependent on the amount of human La protein expressed in the respective cell line. Moreover, acceleration of viral …

virusesImmunologyHerpesvirus 1 Humanmedicine.disease_causeTransfectionVirus ReplicationAutoantigensVirus3T3 cellsSingle-stranded binding proteinMicemedicineImmunology and AllergyAnimalsHumansbiologyTransfection3T3 CellsOriginal ArticlesHerpes simplex virusmedicine.anatomical_structureViral replicationGene Expression RegulationRibonucleoproteinsCytoplasmCell cultureImmunologybiology.proteinClinical and experimental immunology
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Single amino acid substitutions in the glycoprotein B carboxy terminus influence the fusion from without property of herpes simplex virus type 1.

1995

Syncytial mutations of herpes simplex virus type 1 (HSV-1) strains ANG, ANG path, HFEM, tsB5 and HSZP cause extensive cell fusion and were mapped to the cytoplasmic domain of glycoprotein B (gB), within the syn 3 locus. These strains are so far the only ones which show the phenotype ‘fusion from without’ (FFWO): 60 min after infection with high m.o.i., cells in a tissue culture are fused without transcription and translation of the viral genome. In this report we detected, using the recombinants 27/III and K-7, that an amino acid exchange from Ala to Val at aa position 854 of gB is the main determinant for FFWO activity of strains ANG, ANG path and recombinant K-7. The transfer of this muta…

virusesMutantRestriction MappingEnzyme-Linked Immunosorbent AssayHerpesvirus 1 HumanBiologymedicine.disease_causeKidneylaw.inventionCell FusionCytopathogenic Effect ViralViral Envelope ProteinslawVirologyCyclosporin aCricetinaeChlorocebus aethiopsmedicineBaby hamster kidney cellAnimalsAmino Acid SequenceAmino AcidsPeptide sequenceVero CellsRecombination GeneticCell fusionAlanineValineVirologyHerpes simplex virusPhenotypeRecombinant DNAVero cellThe Journal of general virology
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Colonization of adrenal glands and ovaries of mice by variants of HSV 1 and 2

1991

The herpes simplex virus (HSV)-infected mouse model was used to correlate histopathological lesions in adrenal glands and ovaries with the localisation of viral nucleic acids and viral antigens, employing in situ hybridization and immunohistochemistry. In the adrenals, the lesions were mainly restricted to the zona fasciculata and the zona reticularis, sometimes extending to the medulla. In the ovaries, lesions were detected in follicles and in the stroma. During the course of infection, HSV nucleic acids could be detected earlier than HSV proteins. Next to the center of necrotic foci mainly HSV proteins were detected, whereas peripheral cells were found to contain viral nucleic acids. In s…

virusesOvaryIn situ hybridizationBiologymedicine.disease_causeVirusMiceZona fasciculataVirologyAdrenal GlandsmedicineAnimalsAntigens ViralOvaryNucleic Acid HybridizationHerpes SimplexGeneral MedicineImmunohistochemistryVirologymedicine.anatomical_structureHerpes simplex virusDNA ViralNucleic acidImmunohistochemistryFemaleDNA ProbesZona reticularisArchives of Virology
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Quantitative microscopy reveals stepwise alteration of chromatin structure during herpesvirus infection

2019

During lytic herpes simplex virus 1 (HSV-1) infection, the expansion of the viral replication compartments leads to an enrichment of the host chromatin in the peripheral nucleoplasm. We have shown previously that HSV-1 infection induces the formation of channels through the compacted peripheral chromatin. Here, we used three-dimensional confocal and expansion microscopy, soft X-ray tomography, electron microscopy, and random walk simulations to analyze the kinetics of host chromatin redistribution and capsid localization relative to their egress site at the nuclear envelope. Our data demonstrated a gradual increase in chromatin marginalization, and the kinetics of chromatin smoothening arou…

viruseslcsh:QR1-502Herpesvirus 1 HumanmikroskopiaVirus ReplicationinfektiotElectronMicrobiologylcsh:MicrobiologyArticleFluorescenceCell LineBiokemia solu- ja molekyylibiologia - Biochemistry cell and molecular biologyherpes simplex -virustumaChlorocebus aethiopsAnimalsHumansherpesviruksetVero CellsTomographyVirus ReleaseCell NucleusMicroscopyTomography X-RayHerpesvirus 1nuclear egressHerpesviridae InfectionsHSV-1ChromatinMicroscopy ElectronInfectious DiseasesMicroscopy FluorescencetumaegressKasvibiologia mikrobiologia virologia - Plant biology microbiology virologyX-RaykromatiiniSexually Transmitted InfectionschromatinInfectionHuman
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Enhancement by TNF-alpha of reactivation and replication of latent herpes simplex virus from trigeminal ganglia of mice.

1995

The influence of tumor-necrosis-factor-alpha (TNF-alpha), granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukine-1 (IL-1) and IL-3 on the in vitro reactivation frequency and replication rate of trigeminal ganglia of mice latently infected with herpes simplex virus (HSV) strain KOS was studied. It could be demonstrated that TNF-alpha and possibility GM-CSF, but not IL-1 and IL-3, enhanced the reactivation frequency and replication of HSV. Interferon alpha/beta (IFN alpha/beta) prevented reactivation and replication.

virusesmedicine.medical_treatmentHerpesvirus 1 HumanBiologymedicine.disease_causeVirus ReplicationVirusHerpesviridaeMiceInterferonVirologyAlphaherpesvirinaeChlorocebus aethiopsmedicineAnimalsHumansVero CellsMice Inbred BALB CTumor Necrosis Factor-alphaGranulocyte-Macrophage Colony-Stimulating FactorInterferon-alphaGeneral MedicineInterferon-betabiology.organism_classificationVirologyIn vitroVirus LatencyCytokineHerpes simplex virusViral replicationTrigeminal GanglionInterleukin-3Virus Activationmedicine.drugInterleukin-1Archives of virology
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