Leveraging Pathogen-Host Networks to Identify Virus-specific and Estradiol-regulated Mechanisms during Respiratory Infection
利用病原体宿主网络来识别呼吸道感染期间的病毒特异性和雌二醇调节机制
基本信息
- 批准号:10741119
- 负责人:
- 金额:$ 25.35万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2023
- 资助国家:美国
- 起止时间:2023-06-09 至 2025-05-31
- 项目状态:未结题
- 来源:
- 关键词:2019-nCoVAddressAdoptionAffectAge YearsAlgorithmsAutomobile DrivingBindingBioinformaticsCOVID-19CRISPR screenCellsCessation of lifeCodeCommunicable DiseasesCommunitiesComputer AnalysisDataData SetDevelopmentDiseaseDrug resistanceEpidemiologyEpithelial CellsEstradiolFemaleFutureGene ExpressionGenomicsGoalsGonadal Steroid HormonesHormonesHospitalizationHumanImmuneImmune responseInfectionInfectious Diseases ResearchInflammatoryInflammatory ResponseInfluenzaInfluenza A Virus, H1N1 SubtypeInfluenza A Virus, H3N2 SubtypeIntegration Host FactorsKnowledgeLinkMediatingMolecularMorbidity - disease rateNasal EpitheliumNational Institute of Allergy and Infectious DiseaseNatural regenerationNosePathway interactionsPatientsPoliciesProcessProteinsPublishingResearchRespiratory Tract InfectionsSignal TransductionSmall Interfering RNATimeValidationViral Load resultVirusVirus ReplicationWomanWorkcohortdrug candidateeffectiveness evaluationexperiencehuman datain silicoinfluenza infectioninfluenzavirusmathematical modelmenmolecular drug targetmortalitynovelpandemic diseasepathogenpatient variabilitypressureprogramsrespiratoryrespiratory infection virusrespiratory virusresponseseasonal influenzasecondary analysissextherapeutic candidatetherapeutic targettherapy developmentvirus host interactionwhole genomeyoung adult
项目摘要
ABSTRACT
Respiratory viruses, such as influenza and SARS-CoV-2, interact with distinct molecular pathways in human
cells to promote virus replication and alter immune activity. When considering patient cohort variability, morbidity
and mortality are often higher for women than men for select influenza virus infections, exemplified in the 2009
H1N1 pandemic. Estradiol, a major sex hormone, has been shown to impact virus replication in a sex-specific
manner. Yet much remains unknown as to the pathways different viruses engage to promote infection and alter
immune activity or what pathways link estradiol activity to virus replication. This research program uses recently
developed bioinformatics algorithms and NIAID-supported, published datasets in order to reveal new pathways
and molecules involved in infection with influenza viruses and SAR-CoV-2 (Aim 1) and in infection in respiratory
cells derived from women and treated with estradiol (Aim 2). More specifically, we will use two dynamic network
perturbation algorithms, ProTINA and DeltaNeTS+, to create dynamic mathematical models of intracellular
signaling in order to predict important disease modulators. Dynamic network perturbation analysis will be applied
to virus-specific, virus-host interaction networks and host gene expression data induced by each virus. For Aim
2, we have identified gene expression data from influenza-infected nasal cells from female donors that are
pretreated with estradiol. We will validate ProTINA’s and DeltaNeTS+ ability to identify host factors of virus
replication using results from published siRNA- and CRISPR-based screens. After the validation, we will perform
an in-depth characterization of the most significant proteins identified in order to generate new hypothesis on the
host pathways that are involved in infection with different respiratory viruses or that interact with estradiol during
infection.
摘要
项目成果
期刊论文数量(0)
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Jason Edward Shoemaker其他文献
Jason Edward Shoemaker的其他文献
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{{ truncateString('Jason Edward Shoemaker', 18)}}的其他基金
Sex-specific Immune Responses to Severe Influenza Virus Infection
对严重流感病毒感染的性别特异性免疫反应
- 批准号:
10310516 - 财政年份:2020
- 资助金额:
$ 25.35万 - 项目类别:
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