Contribution of IL-32 gene expression to viral persistence
IL-32 基因表达对病毒持久性的贡献
基本信息
- 批准号:10177863
- 负责人:
- 金额:$ 18.95万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2020
- 资助国家:美国
- 起止时间:2020-06-03 至 2023-05-31
- 项目状态:已结题
- 来源:
- 关键词:AffinityAntibodiesAntiviral AgentsAntiviral ResponseAvidityBiomedical EngineeringCardiac MyocytesCardiomyopathiesCell Culture TechniquesCell LineCell NucleusCellsChronicCollaborationsComplementary DNACoxsackie VirusesCoxsackievirus InfectionsCulture MediaCytolysisCytoplasmDevelopmentEpithelial CellsGene ExpressionGene Expression ProfilingGenesGenotypeGoalsGrantHela CellsHumanHuman poliovirusImmuneImmunityInfectionInflammationInnate Immune ResponseInterferon-alphaInterferon-betaInterferonsKnock-outKnowledgeMeasles virusMediator of activation proteinModelingMolecularNonlyticPathway interactionsPharmacologyPhenotypePopulationPredispositionProtein IsoformsProteomicsPublic HealthRNA VirusesRegimenSystemTherapeuticTimeToll-like receptorsUp-RegulationViralViral AntigensVirusVirus DiseasesVirus ReplicationWorkacute infectionbasechronic infectionexperimental studygene discoveryinduced pluripotent stem cellinhibitor/antagonistpathogenpersonalized medicineprogramsprophylacticresponsesensorsingle cell analysistranscriptome
项目摘要
Project Abstract
A case is being made for the utility of MeV persistence in development of lifelong immunity. The thought
is that persistent infection of epithelial cells, in addition to immune cells, may produce virus or viral
antigens to promote affinity maturation of antibodies for a sufficient duration of time that antibodies of
the highest avidity are produced. What governs establishment of a phenotype in an epithelial cell
conducive to establishment of a persistent infection is not known. However, such a cell should be able
to suppress but not eliminate virus multiplication, and virus release must occur by a non-lytic
mechanism to avoid a state of chronic inflammation. Establishing the existence of such persistent-
infection-competent epithelial cells and their gene expression, especially genes involved in control of
virus multiplication, is an essential first step in understanding the molecular basis of viral persistence.
Our single-cell analysis of poliovirus (PV) infection revealed a population of HeLa cells that were quite
proficient at supporting PV multiplication without lysis for as long as 36 h post-infection, which was the
duration of the experiment. We developed a strategy to isolate this sub-population of persistently-
infected cells using standard cell-culture approaches by adding an inhibitor of PV entry to the culture
media. We observed PV persistence for as long as six days post-infection, again the duration of the
experiment. Gene-expression analysis of these persistently-infected cells revealed a near-complete
suppression of sensors of viruses and other pathogens, including Toll-like receptors and “toll-free”
(cytosolic) receptors18. The gene for IL-32 was induced 7 fold (P-value <0.001). IL-32 has been
implicated in antiviral responses that are independent of type I and II interferons (IFNs); however,
effectors of the IL-32-dependent, antiviral pathway have yet to be discovered. The overarching goal of
the program that we will initiate under the auspices of this R21 grant is elucidation of genes, pathways,
and mechanisms required for viral persistence. The first goal of this application is to identify genes that
may contribute to establishment of persistence of CVB3 in human cardiomyocytes. The second goal of
this application is to inspire hypotheses for the mechanism of IL-32 action. These goals will be pursued
as indicated by the following aims: (1) Discover genes contributing to CVB3 persistence in human
cardiomyocytes; and (2) Discover effectors of the IL-32-dependent antiviral state in HeLa cells.
项目摘要
项目成果
期刊论文数量(1)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Robust genome and RNA editing via CRISPR nucleases in PiggyBac systems.
- DOI:10.1016/j.bioactmat.2022.01.046
- 发表时间:2022-08
- 期刊:
- 影响因子:18.9
- 作者:Jiang Y;Hoenisch RC;Chang Y;Bao X;Cameron CE;Lian XL
- 通讯作者:Lian XL
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CRAIG E. CAMERON其他文献
CRAIG E. CAMERON的其他文献
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{{ truncateString('CRAIG E. CAMERON', 18)}}的其他基金
Enteroviral 2C protein as a therapeutic target
肠道病毒2C蛋白作为治疗靶点
- 批准号:
10609524 - 财政年份:2022
- 资助金额:
$ 18.95万 - 项目类别:
Enteroviral 2C protein as a therapeutic target
肠道病毒2C蛋白作为治疗靶点
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10450381 - 财政年份:2022
- 资助金额:
$ 18.95万 - 项目类别:
Optimizing nucleoside analog efficacy with novel exonuclease inhibitors
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10514274 - 财政年份:2022
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$ 18.95万 - 项目类别:
Contribution of IL-32 gene expression to viral persistence
IL-32 基因表达对病毒持久性的贡献
- 批准号:
10057016 - 财政年份:2020
- 资助金额:
$ 18.95万 - 项目类别:
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