THE IMPACT OF IRF-3-DEPENDENT MECHANISMS ON THE REPLICATION AND VIRULENCE OF HSV
IRF-3 依赖性机制对 HSV 复制和毒力的影响
基本信息
- 批准号:8168325
- 负责人:
- 金额:$ 19.99万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2010
- 资助国家:美国
- 起止时间:2010-07-01 至 2011-06-30
- 项目状态:已结题
- 来源:
- 关键词:AgreementCellsComputer Retrieval of Information on Scientific Projects DatabaseDataDendritic CellsFundingGenesGoalsGrantGrowthHerpesvirus 1Immune systemIn VitroInstitutionInterferonsMeasuresMusPathogenesisPathway interactionsPhasePredispositionResearchResearch PersonnelResourcesRoleSimplexvirusSourceSpecificityTestingTissuesUnited States National Institutes of HealthVirulenceVirushuman IRF3 proteinin vivointerferon regulatory factor-3mouse modelresponse
项目摘要
This subproject is one of many research subprojects utilizing the
resources provided by a Center grant funded by NIH/NCRR. The subproject and
investigator (PI) may have received primary funding from another NIH source,
and thus could be represented in other CRISP entries. The institution listed is
for the Center, which is not necessarily the institution for the investigator.
Interferon regulatory factor 3 (IRF3) is critical in the induction phase of the IFN response. Its role, however, in the control of replication of certain viruses, including HSV-1, is enigmatic. A number of HSV genes interfere with the localization and function of IRF-3 in vitro, suggesting that IRF-3 is critical for controlling HSV replication. The deficiency ofIRF-3 would therefore be predicted to preclude the function of early recognition pathways and thereby impact HSV-1 replication. Paradoxically,IRF-3 deficient mice (IRF3-/-) show no increased susceptibility to HSV-1,and no changes in HSV replication in primary IRF-3-/- MEFs have been observed. In agreement with this, we have shown that primary MEFs do not exert such control. Other recent preliminary data, however, showed significantly increased growth of HSV in IRF3-/- dendritic cells, suggesting that cells derived from the immune system exert IRF-3 dependent control over HSV replication.
We reasoned that there were two possible hypotheses to explain these observations. First, that HSV controls IRF-3 activity so completely that, in certain cells, IRF-3 is rendered redundant. Second, that there is a tissue-specificity to the control of HSV replication in vitro and in vivo, and virulence in vivo by IRF-3- dependent mechanisms. The over-arching goal of this proposal is therefore, to test these hypotheses and distinguish between them.
Specific aim 1: To measure and assess the impact of IRF-3- dependent mechanisms upon the replication of HSV in primary cells derived from the immune system in vitro. Specific aim 2: To measure and assess the impact of IRF-3- dependent mechanisms upon the replication and virulence of HSV in mouse models of HSV pathogenesis and latency in vivo.
这个子项目是众多研究子项目之一
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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David A Leib其他文献
David A Leib的其他文献
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{{ truncateString('David A Leib', 18)}}的其他基金
Does Antibody-Dependent Intracellular Neutralization Limit HSV-1 Reactivation?
抗体依赖性细胞内中和是否会限制 HSV-1 重新激活?
- 批准号:
10573477 - 财政年份:2022
- 资助金额:
$ 19.99万 - 项目类别:
Project 3 - Innate immunity and the HSV lytic/latent balance
项目 3 - 先天免疫和 HSV 裂解/潜伏平衡
- 批准号:
10226132 - 财政年份:2013
- 资助金额:
$ 19.99万 - 项目类别:
Project 3 - Innate immunity and the HSV lytic/latent balance
项目 3 - 先天免疫和 HSV 裂解/潜伏平衡
- 批准号:
10460512 - 财政年份:2013
- 资助金额:
$ 19.99万 - 项目类别:
Project 3 - Innate immunity and the HSV lytic/latent balance
项目 3 - 先天免疫和 HSV 裂解/潜伏平衡
- 批准号:
10686369 - 财政年份:2013
- 资助金额:
$ 19.99万 - 项目类别:
Project 3 - Innate immunity and the HSV lytic/latent balance
项目 3 - 先天免疫和 HSV 裂解/潜伏平衡
- 批准号:
9791978 - 财政年份:2013
- 资助金额:
$ 19.99万 - 项目类别:
Bacterial artificial chromosomes for HSV genomics
用于 HSV 基因组学的细菌人工染色体
- 批准号:
6506060 - 财政年份:2002
- 资助金额:
$ 19.99万 - 项目类别:
Bacterial artificial chromosomes for HSV genomics
用于 HSV 基因组学的细菌人工染色体
- 批准号:
6765969 - 财政年份:2002
- 资助金额:
$ 19.99万 - 项目类别:
Bacterial artificial chromosomes for HSV genomics
用于 HSV 基因组学的细菌人工染色体
- 批准号:
6616809 - 财政年份:2002
- 资助金额:
$ 19.99万 - 项目类别:
HSV INDUCED RNA DEGRADATION AND PATHOGENESIS
HSV 诱导的 RNA 降解和发病机制
- 批准号:
2711121 - 财政年份:1994
- 资助金额:
$ 19.99万 - 项目类别:
HSV INDUCED RNA DEGRADATION AND PATHOGENESIS
HSV 诱导的 RNA 降解和发病机制
- 批准号:
2888450 - 财政年份:1994
- 资助金额:
$ 19.99万 - 项目类别:
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