Search results for "viral protein"

showing 10 items of 182 documents

Positive Role of the MHC Class-I Antigen Presentation Regulator m04/gp34 of Murine Cytomegalovirus in Antiviral Protection by CD8 T Cells

2020

Murine cytomegalovirus (mCMV) codes for MHC class-I trafficking modulators m04/gp34, m06/gp48, and m152/gp40. By interacting with the MHC class-Iα chain, these proteins disconnect peptide-loaded MHC class-I (pMHC-I) complexes from the constitutive vesicular flow to the cell surface. Based on the assumption that all three inhibit antigen presentation, and thus the recognition of infected cells by CD8 T cells, they were referred to as “immunoevasins.” Improved antigen presentation mediated by m04 in the presence of m152 after infection with deletion mutant mCMV-Δm06W, compared to mCMV-Δm04m06 expressing only m152, led us to propose renaming these molecules “viral regulators of antigen present…

0301 basic medicineMicrobiology (medical)BAC mutagenesisMuromegalovirusAdoptive cell transfer030106 microbiologyImmunologyAntigen presentationMutantlcsh:QR1-502CD8 T cellsPeptide bindingCD8-Positive T-LymphocytesMajor histocompatibility complexAntiviral AgentsMicrobiologylcsh:MicrobiologyMiceViral Proteins03 medical and health sciencesCellular and Infection MicrobiologyMHC class IAnimalsCytotoxic T cellnext-generation sequencing (NGS)adoptive cell transferimmune evasionAntigen PresentationMembrane GlycoproteinsbiologyMHC class I antigenHistocompatibility Antigens Class IimmunoevasinBrief Research ReportCell biology030104 developmental biologyInfectious Diseasesbiology.proteinrecombinant virusFrontiers in Cellular and Infection Microbiology
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Structure of AP205 Coat Protein Reveals Circular Permutation in ssRNA Bacteriophages.

2016

We are thankful to the MAX-lab staff for their support during our visit at the synchrotron.; International audience; AP205 is a single-stranded RNA bacteriophage that has a coat protein sequence not similar to any other known single-stranded RNA phage. Here, we report an atomic-resolution model of the AP205 virus-like particle based on a crystal structure of an unassembled coat protein dimer and a cryo-electron microscopy reconstruction of the assembled particle, together with secondary structure information from site-specific solid-state NMR data. The AP205 coat protein dimer adopts the conserved Leviviridae coat protein fold except for the N-terminal region, which forms a beta-hairpin in …

0301 basic medicineModels MolecularRNA bacteriophageViral proteinCryo-electron microscopyProtein Conformation010402 general chemistrymedicine.disease_causeCrystallography X-Ray01 natural sciencesvirus-like particleBacteriophage03 medical and health sciencesStructural Biology[CHIM.ANAL]Chemical Sciences/Analytical chemistryLeviviridaemedicineRNA VirusesBacteriophages[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]Molecular BiologyProtein secondary structurebiologyCryoelectron MicroscopyRNA[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologycircular permutationRNA PhagesCircular permutation in proteinsbiology.organism_classification3. Good health0104 chemical sciencesCrystallography030104 developmental biologycoat proteinBiophysicsLeviviridaeCapsid ProteinsJournal of molecular biology
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Human molecular chaperones share with SARS-CoV-2 antigenic epitopes potentially capable of eliciting autoimmunity against endothelial cells: possible…

2020

Severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), the cause of COVID-19 disease, has the potential to elicit autoimmunity because mimicry of human molecular chaperones by viral proteins. We compared viral proteins with human molecular chaperones, many of which are heat shock proteins, to determine if they share amino acid-sequence segments with immunogenic-antigenic potential, which can elicit cross-reactive antibodies and effector immune cells with the capacity to damage-destroy human cells by a mechanism of autoimmunity. We identified the chaperones that can putatively participate in molecular mimicry phenomena after SARS-CoV-2 infection, focusing on those for which endotheli…

0301 basic medicineMolecular chaperonesShort CommunicationPneumonia ViralAutoimmunityBiologymedicine.disease_causeAutoantigensBiochemistryEpitopeAutoimmunity03 medical and health sciencesBetacoronavirusViral Proteins0302 clinical medicineImmune systemEndothelialitisAntigenHeat shock proteinmedicineHumansSevere acute respiratory syndrome coronavirus 2Amino Acid SequenceDatabases ProteinPandemicsHeat-Shock ProteinsEffectorImmunodominant EpitopesSARS-CoV-2Settore BIO/16 - Anatomia UmanaEndothelial CellsCOVID-19Cell BiologyCell biologyEndothelial stem cellMolecular mimicry030104 developmental biologyCoronavirus Infections030217 neurology & neurosurgeryMolecular mimicryCell Stress and Chaperones
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Peptide Processing Is Critical for T-Cell Memory Inflation and May Be Optimized to Improve Immune Protection by CMV-Based Vaccine Vectors.

2016

Cytomegalovirus (CMV) elicits long-term T-cell immunity of unparalleled strength, which has allowed the development of highly protective CMV-based vaccine vectors. Counterintuitively, experimental vaccines encoding a single MHC-I restricted epitope offered better immune protection than those expressing entire proteins, including the same epitope. To clarify this conundrum, we generated recombinant murine CMVs (MCMVs) encoding well-characterized MHC-I epitopes at different positions within viral genes and observed strong immune responses and protection against viruses and tumor growth when the epitopes were expressed at the protein C-terminus. We used the M45-encoded conventional epitope HGI…

0301 basic medicineMuromegalovirusEpitopes T-LymphocyteCD8-Positive T-LymphocytesLymphocyte ActivationPathology and Laboratory MedicineBiochemistryEpitopeMass SpectrometryMiceWhite Blood Cells0302 clinical medicineAnimal CellsMedicine and Health SciencesCytotoxic T celllcsh:QH301-705.5Antigens ViralImmune ResponseStainingVaccines SyntheticbiologyT CellsCell StainingHerpesviridae InfectionsFlow CytometryRecombinant Proteins3. Good healthmedicine.anatomical_structureMedical MicrobiologyViral PathogensVirusesHuman CytomegalovirusCellular TypesPathogensResearch Articlelcsh:Immunologic diseases. AllergyHerpesvirusesT cellImmune CellsAntigen presentationImmunologyCytotoxic T cellsMajor histocompatibility complexResearch and Analysis MethodsMicrobiology03 medical and health sciencesViral ProteinsImmune systemAntigenVirologyGeneticsmedicineAnimalsAntigen-presenting cellMolecular Biology TechniquesMolecular BiologyMicrobial PathogensBlood CellsImmunodominant EpitopesOrganismsBiology and Life SciencesProteinsViral VaccinesCell BiologyVirology030104 developmental biologylcsh:Biology (General)Specimen Preparation and Treatmentbiology.proteinMutagenesis Site-DirectedParasitologylcsh:RC581-607PeptidesDNA virusesImmunologic Memory030215 immunologyChromatography LiquidCloningPLoS pathogens
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The murine cytomegalovirus M35 protein antagonizes type I IFN induction downstream of pattern recognition receptors by targeting NF-κB mediated trans…

2017

The type I interferon (IFN) response is imperative for the establishment of the early antiviral immune response. Here we report the identification of the first type I IFN antagonist encoded by murine cytomegalovirus (MCMV) that shuts down signaling following pattern recognition receptor (PRR) sensing. Screening of an MCMV open reading frame (ORF) library identified M35 as a novel and strong negative modulator of IFNβ promoter induction following activation of both RNA and DNA cytoplasmic PRR. Additionally, M35 inhibits the proinflammatory cytokine response downstream of Toll-like receptors (TLR). Using a series of luciferase-based reporters with specific transcription factor binding sites, …

0301 basic medicineMuromegalovirusPhysiologymedicine.disease_causeBiochemistrychemistry.chemical_compoundMiceWhite Blood Cells0302 clinical medicineCell SignalingTranscription (biology)InterferonAnimal CellsImmune PhysiologyMedicine and Health SciencesMembrane Receptor SignalingBiology (General)Enzyme-Linked ImmunoassaysReceptorConnective Tissue CellsbiologyToll-Like ReceptorsPattern recognition receptorNF-kappa BImmune Receptor SignalingEnzymesThe murine cytomegalovirus M35 protein antagonizes type I IFN induction downstream of pattern recognition receptors by targeting NF-κB mediated transcription.Connective TissueReceptors Pattern RecognitionCytomegalovirus InfectionsInterferon Type ISignal transductionCellular TypesAnatomyBIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti.OxidoreductasesLuciferasemedicine.drugProtein BindingSignal TransductionResearch ArticleViral proteinQH301-705.5Immune CellsImmunologyResearch and Analysis MethodsTransfectionMicrobiology03 medical and health sciencesViral ProteinsMuromegalovirusVirologyGeneticsmedicineAnimalsImmunoassaysMolecular Biology TechniquesMolecular BiologyBlood CellsMacrophagesBIOMEDICINE AND HEALTHCARE. Basic Medical Sciences.Biology and Life SciencesProteinsNF-κBInterferon-betaCell BiologyRC581-607Fibroblastsbiology.organism_classificationMolecular biology030104 developmental biologyBiological TissuechemistryEnzymologyImmunologic TechniquesParasitologyInterferonsImmunologic diseases. AllergySpleen030215 immunology
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Human norovirus hyper-mutation revealed by ultra-deep sequencing

2016

Human noroviruses (NoVs) are a major cause of gastroenteritis worldwide. It is thought that, similar to other RNA viruses, high mutation rates allow NoVs to evolve fast and to undergo rapid immune escape at the population level. However, the rate and spectrum of spontaneous mutations of human NoVs have not been quantified previously. Here, we analyzed the intra-patient diversity of the NoV capsid by carrying out RT-PCR and ultra-deep sequencing with 100,000-fold coverage of 16 stool samples from symptomatic patients. This revealed the presence of low-frequency sequences carrying large numbers of U-to-C or A-to-G base transitions, suggesting a role for hyper-mutation in NoV diversity. To mor…

0301 basic medicineMutation rateVirologiaGene ExpressionVirus Replicationmedicine.disease_causeFecesMutation RateHuman genetics[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseasesCloning MolecularComputingMilieux_MISCELLANEOUSCaliciviridae InfectionsGeneticsMutation[SDV.MHEP.ME]Life Sciences [q-bio]/Human health and pathology/Emerging diseasesGenètica humanaHigh-Throughput Nucleotide SequencingGastroenteritisInfectious Diseases[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/VirologyRNA ViralHyper-mutationMicrobiology (medical)RNA virus[SDE.MCG]Environmental Sciences/Global ChangesContext (language use)BiologyTransfectionMicrobiologyArticleDNA sequencingViral Proteins03 medical and health sciences[SDV.EE.ECO]Life Sciences [q-bio]/Ecology environment/EcosystemsVirologyGeneticsmedicineHumansMolecular BiologyGeneEcology Evolution Behavior and Systematics[SDV.EE.SANT]Life Sciences [q-bio]/Ecology environment/HealthBase SequenceNorovirusRNA virusbiology.organism_classificationVirology[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyHEK293 Cells030104 developmental biologyViral replicationNext-generation sequencingNorovirus[SDE.BE]Environmental Sciences/Biodiversity and Ecology
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Chronic intestinal inflammation in mice expressing viral Flip in epithelial cells

2018

Viruses are present in the intestinal microflora and are currently discussed as a potential causative mechanism for the development of inflammatory bowel disease. A number of viruses, such as Human Herpesvirus-8, express homologs to cellular FLIPs, which are major contributors for the regulation of epithelial cell death. In this study we analyzed the consequences of constitutive expression of HHV8-viral FLIP in intestinal epithelial cells (IECs) in mice. Surprisingly, expression of vFlip disrupts tissue homeostasis and induces severe intestinal inflammation. Moreover vFlip(IEC-tg) mice showed reduced Paneth cell numbers, associated with excessive necrotic cell death. On a molecular level vF…

0301 basic medicineNecrosisTransgeneImmunologyInflammationMice TransgenicBiologydigestive systemArticle03 medical and health sciencesMiceNecrosisViral ProteinsmedicineImmunology and AllergyAnimalsHomeostasisHumansTissue homeostasisCells CulturedRegulation of gene expressionMice KnockoutNF-kappa BHerpesviridae InfectionsInflammatory Bowel DiseasesEpitheliumCell biologyI-kappa B KinaseIntestines030104 developmental biologymedicine.anatomical_structureEnterocytesGene Expression RegulationFlipPaneth cellHerpesvirus 8 Humanmedicine.symptom
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The role of spatial structure in the evolution of viral innate immunity evasion: A diffusion-reaction cellular automaton model

2020

Most viruses have evolved strategies for preventing interferon (IFN) secretion and evading innate immunity. Recent work has shown that viral shutdown of IFN secretion can be viewed as a social trait, since the ability of a given virus to evade IFN-mediated immunity depends on the phenotype of neighbor viruses. Following this idea, we investigate the role of spatial structure in the evolution of innate immunity evasion. For this, we model IFN signaling and viral spread using a spatially explicit approximation that combines a diffusion-reaction model and cellular automaton. Our results indicate that the benefits of preventing IFN secretion for a virus are strongly determined by spatial struct…

0301 basic medicinePhysiologyApoptosisVirus ReplicationBiochemistryVirionsEpitopes0302 clinical medicineInterferonMedicine and Health SciencesBiology (General)Innate Immune Systemeducation.field_of_studyCell DeathEcology3. Good healthCell biologyPhenotypeComputational Theory and MathematicsCell ProcessesModeling and SimulationViral evolutionHost-Pathogen InteractionsVirusesSignal TransductionResearch Articlemedicine.drugEvolutionary ImmunologyQH301-705.5ImmunologyPopulationViral StructureBiologyAntiviral AgentsMicrobiologyViral EvolutionVirusViral Proteins03 medical and health sciencesCellular and Molecular NeuroscienceImmunityVirologyGeneticsmedicineAnimalsHumansComputer SimulationSocial BehavioreducationMolecular BiologySecretionEcology Evolution Behavior and SystematicsImmune EvasionEvolutionary BiologyInnate immune systemVirionBiology and Life SciencesProteinsCell BiologyEvasion (ethics)Immunity InnateOrganismal Evolution030104 developmental biologyViral replicationImmune SystemMicrobial EvolutionInterferonsPhysiological Processes030217 neurology & neurosurgery
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Parsimonious Scenario for the Emergence of Viroid-Like Replicons De Novo

2019

This article belongs to the Special Issue Viroid-2018: International Conference on Viroids and Viroid-Like RNAs. Viroids are small, non-coding, circular RNA molecules that infect plants. Different hypotheses for their evolutionary origin have been put forward, such as an early emergence in a precellular RNA World or several de novo independent evolutionary origins in plants. Here, we discuss the plausibility of de novo emergence of viroid-like replicons by giving theoretical support to the likelihood of different steps along a parsimonious evolutionary pathway. While Avsunviroidae-like structures are relatively easy to obtain through evolution of a population of random RNA sequences of fixe…

0301 basic medicinePopulation dynamicsViroidMatemáticasvirusesPopulationPospiviroidaelcsh:QR1-502Computational biologycomputational simulationsVirus Replicationlcsh:MicrobiologyArticleNucleic acid secondary structureEvolution MolecularViral Proteins03 medical and health sciences0302 clinical medicineCircular RNAVirologypopulation dynamicsModular evolutionRepliconeducationPolymeraseBiología y BiomedicinaSimple replicatorsComputational simulationseducation.field_of_studyViroidstructure enumerationbiologysimple replicatorsviroidStructure enumerationRNARNA Circularbiology.organism_classificationRNA secondary structureViroids030104 developmental biologyInfectious Diseasesbiology.proteinNucleic Acid ConformationRNA ViralRepliconmodular evolution030217 neurology & neurosurgeryViruses
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Viral Bcl2s' transmembrane domain interact with host Bcl2 proteins to control cellular apoptosis

2020

© The Author(s) 2020.

0301 basic medicineProgrammed cell deathScienceProtein domainGeneral Physics and AstronomyApoptosisBiologyVirus-host interactionsArticleGeneral Biochemistry Genetics and Molecular BiologyFluorescenceCell Line03 medical and health sciences0302 clinical medicineProtein Domainsimmune system diseaseshemic and lymphatic diseasesmedicineHumansAmino Acid SequenceAuthor CorrectionPeptide sequenceneoplasmsMultidisciplinaryVirus–host interactionsQCell MembraneGeneral ChemistryViral proteinsmedicine.diseaseControl cellLymphomaCell biologyVirusTransmembrane domain030104 developmental biologyProto-Oncogene Proteins c-bcl-2Cell cultureApoptosisDoxorubicin030220 oncology & carcinogenesisbiological phenomena cell phenomena and immunityProtein MultimerizationHydrophobic and Hydrophilic InteractionsProteïnesProtein Binding
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