Search results for "host-pathogen interactions"

showing 10 items of 171 documents

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
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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
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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
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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
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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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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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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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The Cytoskeletal Adaptor Obscurin-Like 1 Interacts with the Human Papillomavirus 16 (HPV16) Capsid Protein L2 and Is Required for HPV16 Endocytosis.

2016

ABSTRACT The human papillomavirus (HPV) capsid protein L2 is essential for viral entry. To gain a deeper understanding of the role of L2, we searched for novel cellular L2-interacting proteins. A yeast two-hybrid analysis uncovered the actin-depolymerizing factor gelsolin, the membrane glycoprotein dysadherin, the centrosomal protein 68 (Cep68), and the cytoskeletal adaptor protein obscurin-like 1 protein (OBSL1) as putative L2 binding molecules. Pseudovirus (PsV) infection assays identified OBSL1 as a host factor required for gene transduction by three oncogenic human papillomavirus types, HPV16, HPV18, and HPV31. In addition, we detected OBSL1 expression in cervical tissue sections and no…

0301 basic medicineKeratinocytesvirusesImmunologyEndocytic cycleEndocytosisMicrobiologyClathrinCell Line03 medical and health sciencesTransduction (genetics)TetraspaninViral entryVirologyTwo-Hybrid System TechniquesCaveolinHumansHuman papillomavirus 16biologyPapillomavirus InfectionsSignal transducing adaptor proteinOncogene Proteins ViralVirus InternalizationEndocytosisCell biologyVirus-Cell InteractionsCytoskeletal Proteins030104 developmental biologyInsect ScienceGene Knockdown TechniquesHost-Pathogen Interactionsbiology.proteinCapsid ProteinsHeLa CellsJournal of virology
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