Hijacking of cellular pathways by novel tick-borne phlebovirus
Hijacking of cellular pathways by novel tick-borne phlebovirus
批准号:
9088328
负责人:
Patricia Veronica Aguilar
金额:
$19.26万
依托单位国家:
美国
项目类别:
财政年份:
2015
资助国家:
美国
项目状态:
已结题
起止时间:
2015-06-15 至 2018-05-31
关键词:
Antiviral AgentsAsiaAutophagocytosisCase Fatality RatesCell physiologyCellsChinaConfocal MicroscopyCytoplasmic StructuresDataDegradation PathwayDevelopmentDiseaseEarly EndosomeEndoplasmic ReticulumEndosomesEnvironmentFatality rateFeverFutureGenesGenus PhlebovirusGoalsGolgi ApparatusHealthHeartland virusHost DefenseHumanImmuneImmune responseInfectionInterferon Type IInterferon-betaInterferonsJapanKnowledgeKoreaLeadLigandsMediatingMolecularNatural ImmunityNucleoproteinsOrthobunyavirusOutcomePathogenesisPathway interactionsPatientsPersonsPolymerasePreventive InterventionProcessProteinsRNA VirusesReportingResearchRoleSignal TransductionSignaling ProteinStructureSyndromeTANK-binding kinase 1TRIM25 geneTherapeuticTherapeutic InterventionThrombocytopeniaTicksUbiquitinUbiquitinationUnited StatesVaccinesViral Hemorrhagic FeversViral Nonstructural ProteinsVirusVirus DiseasesVirus Replicationbasecombatdefined contributiongenetic regulatory proteininhibitor/antagonistmonocytemortalitynovelpathogenpreventpromoterresponsesensortherapeutic vaccinetransmission processubiquitin-protein ligasevaccine developmentviral RNAvirus pathogenesis
中文摘要
英文摘要
DESCRIPTION (provided by applicant): The novel bunyavirus Severe Fever Thrombocytopenia Syndrome virus (SFTSV) was recently isolated from patients presenting with fever, thrombocytopenia and hemorrhagic manifestations. An initial case fatality rate of 12-30% has been reported and evidence of person-to-person transmission has also been recently documented. The exact mechanism by which this virus causes disease is still unknown. The possibility of person-to-person transmission, the high fatality rate associated with infection and the recent emergence of Heartland virus, a close relative of SFTSV, highlights the need to increase our knowledge on how these new pathogens cause diseases. Furthermore, it also underscores the need to develop therapeutic interventions against these emerging pathogens. We have determined that the SFTSV nonstructural NSs protein is a potent inhibitor of host interferon (IFN) responses. Astonishingly, we found that the SFTSV nonstructural NSs protein interacts with and relocalizes RIG-I, TRIM25 and TBK1, key components of the Type I IFN response pathway, into NSs-induced cytoplasmic structures in a process that involves ubiquitin and the early endosome pathway. Thus, the goal of this project is to provide a detailed understanding of how these cellular processes are targeted by SFTSV to counteract host innate immune responses and establish infection. Completion of this study will describe a novel immune evasion strategy for subversion of host innate immunity by SFTSV that is distinct from the current paradigm for bunyaviruses. We expect the fundamental information generated in this project will advance the field by defining a novel immune evasion strategy for subversion of host innate immune responses and very likely provide new targets for therapeutic interventions and vaccine development against SFTSV and other related pathogenic RNA viruses.
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