Search results for "Host-Pathogen Interaction"

showing 10 items of 189 documents

Epithelium‐specific MyD88 signaling, but not DCs or macrophages, control acute intestinal infection with Clostridium difficile

2019

Infection with Clostridium difficile is one of the major causes of health care acquired diarrhea and colitis. Signaling though MyD88 downstream of TLRs is critical for initiating the early protective host response in mouse models of C. difficile infection (CDI). In the intestine, MyD88 is expressed in various tissues and cell types, such as the intestinal epithelium and mononuclear phagocytes (MNP), including DC or macrophages. Using a genetic gain-of-function system, we demonstrate here that restricting functional MyD88 signaling to the intestinal epithelium, but also to MNPs is sufficient to protect mice during acute CDI by upregulation of the intestinal barrier function and recruitment o…

0301 basic medicineCell typeImmunologyBiologyMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationmedicineAnimalsImmunology and AllergyIntestinal MucosaColitisEnterocolitis PseudomembranousBarrier functionClostridioides difficileMacrophagesDendritic CellsClostridium difficilemedicine.diseaseIntestinal epitheliumPhenotypeEpitheliumDisease Models Animal030104 developmental biologymedicine.anatomical_structureHost-Pathogen InteractionsMyeloid Differentiation Factor 88ImmunologySignal Transduction030215 immunologyEuropean Journal of Immunology
researchProduct

COVID-19: viral–host interactome analyzed by network based-approach model to study pathogenesis of SARS-CoV-2 infection

2020

AbstractBackgroundEpidemiological, virological and pathogenetic characteristics of SARS-CoV-2 infection are under evaluation. A better understanding of the pathophysiology associated with COVID-19 is crucial to improve treatment modalities and to develop effective prevention strategies. Transcriptomic and proteomic data on the host response against SARS-CoV-2 still have anecdotic character; currently available data from other coronavirus infections are therefore a key source of information.MethodsWe investigated selected molecular aspects of three human coronavirus (HCoV) infections, namely SARS-CoV, MERS-CoV and HCoV-229E, through a network based-approach. A functional analysis of HCoV-hos…

0301 basic medicineChemokinevirusesPneumonia ViralGene regulatory networklcsh:MedicineComputational biologyVirus-host interactomemedicine.disease_causeModels BiologicalInteractomeGeneral Biochemistry Genetics and Molecular BiologyTranscriptomePathogenesis03 medical and health sciencesBetacoronavirus0302 clinical medicineViral Envelope ProteinsProtein Interaction MappingmedicineCoronavirus infectionHumansGene Regulatory NetworksPandemicsGeneCoronavirusVirus–host interactomeMembrane GlycoproteinsInnate immune systembiologySARS-CoV-2Researchlcsh:RCOVID-19virus diseasesGeneral Medicinebiochemical phenomena metabolism and nutritionVirus–host interactome ; COVID-19 ; Coronavirus infection ; Spike glycoproteinPhenotyperespiratory tract diseasescoronavirus infection; spike glycoprotein; virus-host interactome030104 developmental biologySettore MED/38 - PEDIATRIA GENERALE E SPECIALISTICA030220 oncology & carcinogenesisHost-Pathogen Interactionsbiology.proteinSpike glycoproteinCoronavirus InfectionsSignal TransductionJournal of Translational Medicine
researchProduct

Gut microbiota imbalance and colorectal cancer

2016

International audience; The gut microbiota acts as a real organ. The symbiotic interactions between resident micro-organisms and the digestive tract highly contribute to maintain the gut homeostasis. However, alterations to the microbiome caused by environmental changes (e.g., infection, diet and/or lifestyle) can disturb this symbiotic relationship and promote disease, such as inflammatory bowel diseases and cancer. Colorectal cancer is a complex association of tumoral cells, non-neoplastic cells and a large amount of micro-organisms, and the involvement of the microbiota in colorectal carcinogenesis is becoming increasingly clear. Indeed, many changes in the bacterial composition of the g…

0301 basic medicineColorectal cancer[SDV]Life Sciences [q-bio]enterotoxigenic bacteroides-fragilisGut floraCyclomodulin[ SDV.CAN ] Life Sciences [q-bio]/CancerTopic Highlightstreptococcus-gallolyticus infectionbiologyGastrointestinal MicrobiomeGastroenterologyGeneral Medicinecytolethal-distending toxin3. Good healthlactobacillus-acidophilus deficientIntestinesCell Transformation NeoplasticHost-Pathogen InteractionsInflammation MediatorsColorectal NeoplasmsVirulence Factorspolymerase-chain-reaction[SDV.CAN]Life Sciences [q-bio]/CancerGut microbiotaoxidative dna-damageMicrobiologyescherichia-coli strains03 medical and health scienceshelicobacter-pylori infectionmedicineAnimalsHumansMicrobiomeBacteria[ SDV ] Life Sciences [q-bio]inflammatory-bowel-diseaseCancerHelicobacter pyloribiology.organism_classificationmedicine.diseaseStreptococcus bovisColorectal cancerGastrointestinal MicrobiomeHépatologie et Gastroentérologie030104 developmental biologytoll-like receptorsOxidative stressImmunologyHépatology and GastroenterologyDysbiosiscolorectal cancer;gut microbiota;dysbiosis;cyclomodulin;oxidative;stress;enterotoxigenic bacteroides-fragilis;oxidative dna-damage;cytolethal-distending toxin;inflammatory-bowel-disease;streptococcus-gallolyticus infection;lactobacillus-acidophilus;deficient;helicobacter-pylori infection;polymerase-chain-reaction;escherichia-coli strains;toll-like receptorsDysbiosisDNA Damage
researchProduct

SARS-CoV-2 and COVID-19: A genetic, epidemiological, and evolutionary perspective

2020

In less than five months, COVID-19 has spread from a small focus in Wuhan, China, to more than 5 million people in almost every country in the world, dominating the concern of most governments and public health systems. The social and political distresses caused by this epidemic will certainly impact our world for a long time to come. Here, we synthesize lessons from a range of scientific perspectives rooted in epidemiology, virology, genetics, ecology and evolutionary biology so as to provide perspective on how this pandemic started, how it is developing, and how best we can stop it.

0301 basic medicineEconomic growth[SDV]Life Sciences [q-bio]Gene ExpressionSeverity of Illness IndexDisease OutbreaksBiological CoevolutionChiropteraPandemicEpidemiologyPhylogenyComputingMilieux_MISCELLANEOUSEutheriaPhylodynamics3. Good healthEuropeInfectious DiseasesHost susceptibilityHost-Pathogen InteractionsSpike Glycoprotein CoronavirusAngiotensin-Converting Enzyme 2Coronavirus InfectionsMicrobiology (medical)medicine.medical_specialtyAsiaCoronavirus disease 2019 (COVID-19)Pneumonia Viral030106 microbiologyFILOGENIAPeptidyl-Dipeptidase ABiologyMicrobiologyArticleBetacoronavirus03 medical and health sciencesPoliticsGeneticsmedicineAnimalsHumansChinaPandemicsMolecular BiologyEcology Evolution Behavior and SystematicsSARS-CoV-2Public healthPerspective (graphical)COVID-19Immunity InnateCoronavirusImmune system030104 developmental biologyViral phylodynamicsNorth AmericaCoevolution
researchProduct

Virus-host interactome: Putting the accent on how it changes

2017

[EN] Viral infections are extremely complex processes that could only be well understood by precisely characterizing the interaction networks between the virus and the host components. In recent years, much effort has gone in this directionwith the aimof unveiling themolecular basis of viral pathology. These networks are mostly formed by viral and host proteins, and are expected to be dynamic bothwith time and space (i.e., with the progression of infection, as well as with the virus and host genotypes; what we call plastodynamic). This largely overlooked spatio-temporal evolution urgently calls for a change both in the conceptual paradigms and experimental techniques used so far to characte…

0301 basic medicineEvolutionSystems biologyBiophysicsComplex diseaseDiseaseComputational biologyBiologyBioinformaticsBiochemistryInteractomeVirusViral Proteins03 medical and health sciencesSpatio-Temporal AnalysisProtein networkVirologyStress (linguistics)AnimalsHumansProtein Interaction MapsVirus host030102 biochemistry & molecular biologyHost (biology)030104 developmental biologyVirus DiseasesHost-Pathogen InteractionsSystems biologyJournal of Proteomics
researchProduct

Coinfection outcome in an opportunistic pathogen depends on the inter-strain interactions

2017

Background In nature, organisms are commonly coinfected by two or more parasite strains, which has been shown to influence disease virulence. Yet, the effects of coinfections of environmental opportunistic pathogens on disease outcome are still poorly known, although as host-generalists they are highly likely to participate in coinfections. We asked whether coinfection with conspecific opportunistic strains leads to changes in virulence, and if these changes are associated with bacterial growth or interference competition. We infected zebra fish (Danio rerio) with three geographically and/or temporally distant environmental opportunist Flavobacterium columnare strains in single and in coinf…

0301 basic medicineGenotypemedia_common.quotation_subjectVirulencecooperationgenotyyppiFlavobacteriumIntraspecific competitionCompetition (biology)Host SpecificityMicrobiology03 medical and health sciencesFlavobacterium columnareFish DiseasesgenotypesGenotypemedicineAnimalsseeprakalaPathogenZebrafishEcology Evolution Behavior and Systematicsmedia_commonInhibitionbiologyCompetitionVirulenceHost (biology)Zebra fishCoinfectionvirulenssibiology.organism_classificationmedicine.diseaseinhibitionCooperation030104 developmental biologyFlavobacterium columnareHost-Pathogen InteractionsCoinfectioncompetitionResearch ArticleBMC Evolutionary Biology
researchProduct

Microvesicles released from Giardia intestinalis disturb host-pathogen response in vitro

2017

Giardia intestinalis (G.I), is an anaerobic protozoan and the aetiological agent of giardiasis, a diarrhoea present worldwide and associated with poverty. G.I has a simple life cycle alternating between cyst and trophozoite. Cysts are transmitted orally to the stomach and transform to trophozoites in the intestine by a multifactorial process. Recently, microvesicles (MVs) have been found to be released from a wide range of eukaryotic cells. We have observed a release of MVs during the life cycle of G.I., identifying MVs from active trophozoites and from trophozoites differentiating to the cyst form. The aim of the current work was to investigate the role of MVs from G.I in the pathogenesis …

0301 basic medicineGiardiasisHistologydewey610Biologymedicine.disease_causePathology and Forensic MedicineMicrobiologyPathogenesis03 medical and health sciencesExtracellular VesiclesCell-Derived MicroparticlesmedicineGiardia lambliaAnimalsHumansPathogenLipid raftdewey570Innate immunityInnate immune systemParasite-host cell interactionsCell BiologyGeneral Medicine030108 mycology & parasitologyGiardia intestinalisExtracellular vesiclesIn vitroMicrovesiclesImmunity InnateDiarrhoea030104 developmental biologyHost-Pathogen InteractionsCaco-2 CellsGiardia lambliaBiogenesisMicrovesicles
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct