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showing 10 items of 2898 documents

Hepatitis B Virus Subverts the Autophagy Elongation Complex Atg5-12/16L1 and Does Not Require Atg8/LC3 Lipidation for Viral Maturation

2018

ABSTRACT Previous studies indicated that hepatitis B virus (HBV) stimulates autophagy to favor its production. To understand how HBV co-opts autophagy as a proviral machinery, we studied the roles of key autophagy proteins in HBV-replicating liver cell cultures. RNA interference-mediated silencing of Atg5, Atg12, and Atg16L1, which promote autophagophore expansion and LC3 membrane conjugation, interfered with viral core/nucleocapsid (NC) formation/stability and strongly diminished virus yields. Concomitantly, the core/NC membrane association and their sorting to envelope-positive compartments were perturbed. A close inspection of the HBV/autophagy cross talk revealed that the virus depended…

0301 basic medicineHepatitis B virusATG8Autophagosome maturationImmunologyATG5Autophagy-Related ProteinsBiologymedicine.disease_causeVirus ReplicationMicrobiologyVirusAutophagy-Related Protein 5ATG1203 medical and health sciencesVirologyCell Line TumormedicineAutophagyHumansHepatitis B virusAutophagyAutophagy-Related Protein 8 FamilyHepatitis BCell biologyVirus-Cell Interactions030104 developmental biologyViral replicationInsect ScienceGene Knockdown TechniquesMultiprotein ComplexesMicrotubule-Associated ProteinsAutophagy-Related Protein 12
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Rab33B Controls Hepatitis B Virus Assembly by Regulating Core Membrane Association and Nucleocapsid Processing

2017

Many viruses take advantage of cellular trafficking machineries to assemble and release new infectious particles. Using RNA interference (RNAi), we demonstrate that the Golgi/autophagosome-associated Rab33B is required for hepatitis B virus (HBV) propagation in hepatoma cell lines. While Rab33B is dispensable for the secretion of HBV subviral envelope particles, its knockdown reduced the virus yield to 20% and inhibited nucleocapsid (NC) formation and/or NC trafficking. The overexpression of a GDP-restricted Rab33B mutant phenocopied the effect of deficit Rab33B, indicating that Rab33B-specific effector proteins may be involved. Moreover, we found that HBV replication enhanced Rab33B expres…

0301 basic medicineHepatitis B virusBiologymedicine.disease_causeVirusArticleCell LineCell membraneRab33B03 medical and health sciencesnucleocapsid assemblyTranscription (biology)RNA interferenceVirologymedicineHumansSecretionNucleocapsidcore/capsid membrane associationHepatitis B virus030102 biochemistry & molecular biologyEffectorVirus AssemblyCell MembraneVirologyHepatitis B Core Antigenshepatitis B virus; Rab GTPase; Rab33B; core/capsid membrane association; nucleocapsid assembly; virus traffickingTransport proteinProtein Transport030104 developmental biologyInfectious Diseasesmedicine.anatomical_structurevirus traffickingrab GTP-Binding ProteinsHost-Pathogen InteractionsHepatocytesRab GTPaseViruses; Volume 9; Issue 6; Pages: 157
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The immunoglobulin γ marker 17 allotype and KIR/HLA genes prevent the development of chronic hepatitis B in humans

2020

Hepatitis B virus (HBV) infection causes a self-limiting disease in most individuals. However, < 10% of infected subjects develop a chronic disease. Genetic host variability of polymorphic genes at the interface of innate and acquired immunity, such as killer immunoglobulin-like receptors (KIR), their human leucocyte antigen (HLA) and IgG allotypes (GM), could explain this different clinical picture. We previously showed a protective role of the KIR2DL3 gene for the development of chronic hepatitis B (CHB), and a detrimental role of the KIR ligand groups, HLA-A-Bw4 and HLA-C2. We have expanded the previous analysis genotyping patients for GM23 and GM3/17 allotypes. The comparison of the …

0301 basic medicineHepatitis B virusKIR LigandImmunologyhepatitis B viruHuman leukocyte antigenHLA-C Antigensmedicine.disease_causeRisk Assessment03 medical and health sciences0302 clinical medicineHepatitis B ChronicGene FrequencyImmunoglobulin Gm AllotypesRisk Factorskiller immunoglobulin-like receptorImmunology and AllergyMedicineHumansGenetic Predisposition to DiseaseGenotypingHepatitis B virusSettore MED/04 - Patologia Generalebiologybusiness.industryOriginal ArticlesProtective FactorsAcquired immune systemAllotypeγ marker030104 developmental biologyPhenotypeHLA-B AntigensReceptors KIR2DL3Case-Control StudiesImmunologyHost-Pathogen Interactionsbiology.proteinGene polymorphismAntibodyhepatitis B virus; human leucocyte antigen; killer immunoglobulin-like receptor; ? markerbusiness030215 immunologyhuman leucocyte antigen
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Parasitic wasp-associated symbiont affects plant-mediated species interactions between herbivores

2018

Abstract Microbial mutualistic symbiosis is increasingly recognised as a hidden driving force in the ecology of plant–insect interactions. Although plant-associated and herbivore-associated symbionts clearly affect interactions between plants and herbivores, the effects of symbionts associated with higher trophic levels has been largely overlooked. At the third-trophic level, parasitic wasps are a common group of insects that can inject symbiotic viruses (polydnaviruses) and venom into their herbivorous hosts to support parasitoid offspring development. Here, we show that such third-trophic level symbionts act in combination with venom to affect plant-mediated interactions by reducing colon…

0301 basic medicineHerbivore colonisationInsecta[SDV]Life Sciences [q-bio]tritrophic interactionWaspsVenomParasitoidchenilleLaboratory of EntomologyTrophic levelbiologyEcologyPolydnavirusHost-Parasite Interactionfood and beveragesplant–insect interactionsHerbivore colonisation parasitoid plant–insect interactions polydnaviruses tritrophic interactionsPE&RCsymbiosisParasiteinternationalpolydnaviruse[SDE]Environmental Sciencespolydnavirussymbioseécologie des populationsinteraction plante insecteherbivoreplant–insect interactionHost-Parasite Interactions03 medical and health sciencesSymbiosisAnimalsParasitesHerbivoryguêpeCaterpillarparasitoidEcology Evolution Behavior and SystematicsHerbivoreAnimaltritrophic interactionsfungi15. Life on landplant-insect interactionsLaboratorium voor Entomologiebiology.organism_classificationplant insect interactionherbivore colonisationpolydnavirusesColonisationSettore AGR/11 - Entomologia Generale E Applicata030104 developmental biologycaterpillarEPS
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Overview of the interaction of helminth extracellular vesicles with the host and their potential functions and biological applications.

2021

Helminth Extracellular Vesicles (EVs) have emerged as important mediators in host-parasite communications, participating in the parasite survival and its pathogenic effects. In the last decade, a growing amount of information reporting the isolation and characterization of EVs from different helminth species has appeared, but unfortunately, few reports have focused on functional studies of helminth EVs in different cell lines, organoids or animal models. We here review these in vitro and in vivo studies, which clearly demonstrate that helminths secrete EVs, which affect their environment. Helminth EVs are actively internalized by different cell lines, modulating cellular functions important…

0301 basic medicineHost (biology)ImmunologyCellular functionsHelminthiasisComputational biologyBiologyExtracellular vesiclesHost-Parasite Interactions03 medical and health sciencesExtracellular Vesicles030104 developmental biology0302 clinical medicineImmune systemHelminthsparasitic diseasesHelminthsAnimalsHumansSecretionFunctional studiesInformation reportingMolecular Biology030215 immunologyMolecular immunology
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Role of Immunogenetics in the Outcome of HCMV Infection: Implications for Ageing

2019

The outcome of host-virus interactions is determined by a number of factors, some related to the virus, others to the host, such as environmental factors and genetic factors. Therefore, different individuals vary in their relative susceptibility to infections. Human cytomegalovirus (HCMV) is an important pathogen from a clinical point of view, as it causes significant morbidity and mortality in immunosuppressed or immunosenescent individuals, such as the transplanted patients and the elderly, respectively. It is, therefore, important to understand the mechanisms of virus infection control. In this review, we discuss recent advances in the immunobiology of HCMV-host interactions, with partic…

0301 basic medicineHuman cytomegalovirusAgingCellular immunityvirusesCytomegalovirusReviewlcsh:Chemistry0302 clinical medicineHLA AntigensGenotypeMedicineantibodieslcsh:QH301-705.5SpectroscopyimmunosenescenceImmunity CellularbiologyGeneral MedicineImmunosenescenceGMComputer Science ApplicationsKIRHLAantibodieCytomegalovirus InfectionsHost-Pathogen InteractionsAntibodyGenotypeNKCongenital cytomegalovirus infectionHuman leukocyte antigenelderlyCatalysisVirusInorganic Chemistry03 medical and health sciencesImmunogeneticsAnimalsHumansGenetic Predisposition to DiseasePhysical and Theoretical ChemistryMolecular BiologyHCMVSettore MED/04 - Patologia Generalebusiness.industryOrganic Chemistrymedicine.diseaseImmunity Humoral030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Immunologybiology.proteinbusiness030215 immunology
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Regulatory Interaction between the Cellular Restriction Factor IFI16 and Viral pp65 (pUL83) Modulates Viral Gene Expression and IFI16 Protein Stabili…

2016

ABSTRACT A key player in the intrinsic resistance against human cytomegalovirus (HCMV) is the interferon-γ-inducible protein 16 (IFI16), which behaves as a viral DNA sensor in the first hours postinfection and as a repressor of viral gene transcription in the later stages. Previous studies on HCMV replication demonstrated that IFI16 binds to the viral protein kinase pUL97, undergoes phosphorylation, and relocalizes to the cytoplasm of infected cells. In this study, we demonstrate that the tegument protein pp65 (pUL83) recruits IFI16 to the promoter of the UL54 gene and downregulates viral replication, as shown by use of the HCMV mutant v65Stop, which lacks pp65 expression. Interestingly, at…

0301 basic medicineHuman cytomegalovirusViral proteinviruses030106 microbiologyImmunologyCytomegalovirusDNA-Directed DNA PolymeraseBiologymedicine.disease_causeVirus ReplicationMicrobiologyViral Matrix Proteins03 medical and health sciencesViral ProteinsVirologymedicineHumansNuclear proteinPromoter Regions GeneticGeneCells CulturedViral matrix proteinIFI16Protein Stabilityvirus diseasesNuclear ProteinsViral tegumentmedicine.diseasePhosphoproteinsMolecular biologyVirus-Cell Interactions030104 developmental biologyViral replicationInsect ScienceDNA ViralHost-Pathogen InteractionsProtein BindingJournal of virology
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Tetraspanin CD151 Promotes Initial Events in Human Cytomegalovirus Infection.

2016

ABSTRACT Human cytomegalovirus (HCMV), a betaherpesvirus, can cause life-threatening disease in immunocompromised individuals. Viral envelope glycoproteins that mediate binding to and penetration into target cells have been identified previously. In contrast, cellular proteins supporting HCMV during entry are largely unknown. In order to systematically identify host genes affecting initial steps of HCMV infection, a targeted RNA interference screen of 96 cellular genes was performed in endothelial cells by use of a virus strain expressing the full set of known glycoprotein H and L (gH/gL) complexes. The approach yielded five proviral host factors from different protein families and eight an…

0301 basic medicineHuman cytomegalovirusvirusesImmunologyCytomegalovirusBiologyTetraspanin 24MicrobiologyVirus03 medical and health sciencesViral envelopeTetraspaninViral Envelope ProteinsRNA interferenceVirologymedicineHuman Umbilical Vein Endothelial CellsHumansRNA Small InterferingTropismCells CulturedHost factorchemistry.chemical_classificationFibroblastsVirus Internalizationmedicine.diseaseVirologyVirus-Cell Interactions030104 developmental biologychemistryInsect ScienceRNA InterferenceGlycoproteinGene DeletionJournal of virology
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Regulation of kynurenine biosynthesis during influenza virus infection.

2017

Influenza A viruses (IAVs) remain serious threats to public health because of the shortage of effective means of control. Developing more effective virus control modalities requires better understanding of virus–host interactions. It has previously been shown that IAV induces the production of kynurenine, which suppresses T-cell responses, enhances pain hypersensitivity and disturbs behaviour in infected animals. However, the regulation of kynurenine biosynthesis during IAV infection remains elusive. Here we showed that IAV infection induced expression of interferons (IFNs), which upregulated production of indoleamine-2,3-dioxygenase (IDO1), which catalysed the kynurenine biosynthesis. Furt…

0301 basic medicineIndoleshost-pathogen interactionViral Nonstructural Proteinsmedicine.disease_causeVirus ReplicationBiochemistryinfluenza viruschemistry.chemical_compoundMiceInfluenza A Virus H1N1 SubtypeInterferonOximesinnate immunityLungOxazolesKynurenineRegulation of gene expressionMice Inbred BALB CSulfonamidesTryptophaninterferon3. Good healthHost-Pathogen InteractionsFemaleMetabolic Networks and Pathwaysmedicine.drugHost–pathogen interaction030106 microbiologyPrimary Cell CultureBiologyta3111Antiviral AgentsVirus03 medical and health sciences3-dioxygenase (IDO1)Orthomyxoviridae InfectionsmedicineAnimalsHumansImmunologic FactorsIndoleamine-Pyrrole 23-DioxygenasePyrrolesMolecular BiologyInnate immune systemta1184Macrophagesta1183ta1182Cell BiologyVirologyindoleamine-pyrrole 2Thiazoles030104 developmental biologyHerpes simplex virusViral replicationchemistryGene Expression RegulationInterferonsTranscriptomeKynurenineThe FEBS journal
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Collective properties of viral infectivity

2018

Individual virions typically fail to infect cells. Such decoupling between virions and infectious units is most evident in multicomponent and other segmented viruses, but is also frequent in non-segmented viruses. Despite being a well-known observation, the causes and implications of low single-virion infectivity often remain unclear. In principle, this can originate from intrinsic genetic and/or structural virion defects, but also from host infection barriers that limit early viral proliferation. Hence, viruses may have evolved strategies to increase the per-virion likelihood of establishing successful infections. This can be achieved by adopting spread modes that elevate the multiplicity …

0301 basic medicineInfectivityvirusesBiologyVirus Physiological PhenomenaCellular levelbiochemical phenomena metabolism and nutritionVirus InternalizationVirus ReplicationVirologyMicrovesiclesDefective virusArticle03 medical and health sciences030104 developmental biologyMultiplicity of infectionViral replicationVirion bindingVirus DiseasesVirologyMicrobial InteractionsVirus Physiological Phenomena
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