MODULATION OF INNATE IMMUNE RESPONSES BY CYTOMEGALOVIRUS
巨细胞病毒对先天免疫反应的调节
基本信息
- 批准号:8357775
- 负责人:
- 金额:$ 38.95万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2011
- 资助国家:美国
- 起止时间:2011-05-01 至 2012-04-30
- 项目状态:已结题
- 来源:
- 关键词:CytomegalovirusFundingGenesGrantHumanImmune responseImmune systemInterferonsMacaca mulattaMolecularNational Center for Research ResourcesPrimatesPrincipal InvestigatorProteinsPublishingResearchResearch InfrastructureResourcesSourceTestingUnited States National Institutes of HealthViralViruscostgene inductionhuman IRF3 proteininterferon regulatory factor-3research studyresponse
项目摘要
This subproject is one of many research subprojects utilizing the resources
provided by a Center grant funded by NIH/NCRR. Primary support for the subproject
and the subproject's principal investigator may have been provided by other sources,
including other NIH sources. The Total Cost listed for the subproject likely
represents the estimated amount of Center infrastructure utilized by the subproject,
not direct funding provided by the NCRR grant to the subproject or subproject staff.
The ultimate inability of the immune system to eliminate cytomegalovirus (CMV) from the host is likely due to sophisticated viral evasion mechanisms that target many aspects of the host immune system. In this project, we will try to gain a better understanding of the molecular mechanisms by which CMV modulates the induction of innate immune responses, particularly the interferon response. Specific Aim 1 is to identify how HCMV activates interferon-regulatory factor 3 (IRF3). This aim has been completed and the results have been published. Specific Aims 2 and 3 are to determine how human and rhesus CMV interfere with IRF3-dependent transcriptional induction of interferon-stimulated genes (ISGs). We have tested our original hypothesis that the tegument proteins pp65 and pp71 are responsible for inhibiting IRF3 activation by RhCMV by generating deletion viruses. However, since these viruses still inhibit IRF3 activation, we now hypothesize that RhCMV contains additional IRF3 inhibitory genes. Current experiments are aimed at identifying these genes. In addition, we now explore the inhibition of IFN-dependent ISG induction by RhCMV and we have generated evidence that HCMV also inhibits IRF3 activation.
这个子项目是许多利用资源的研究子项目之一
由NIH/NCRR资助的中心拨款提供。子项目的主要支持
子项目的主要研究者可能是由其他来源提供的,
包括其它NIH来源。 列出的子项目总成本可能
代表子项目使用的中心基础设施的估计数量,
而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。
免疫系统最终无法从宿主中消除巨细胞病毒(CMV)可能是由于靶向宿主免疫系统许多方面的复杂病毒逃避机制。在这个项目中,我们将试图更好地了解CMV调节先天性免疫应答,特别是干扰素应答的分子机制。具体目标1是确定HCMV如何激活干扰素调节因子3(IRF 3)。这一目标已经完成,结果已经公布。 具体目标2和3是确定人和恒河猴CMV如何干扰干扰素刺激基因(ISG)的IRF 3依赖性转录诱导。 我们已经测试了我们最初的假设,即被膜蛋白pp 65和pp 71负责通过产生缺失病毒来抑制RhCMV对IRF 3的激活。然而,由于这些病毒仍然抑制IRF 3激活,我们现在假设RhCMV含有额外的IRF 3抑制基因。目前的实验旨在识别这些基因。此外,我们现在探索的抑制IFN依赖性ISG诱导RhCMV和我们已经产生的证据表明,HCMV也抑制IRF 3激活。
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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Klaus J Fruh其他文献
Klaus J Fruh的其他文献
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{{ truncateString('Klaus J Fruh', 18)}}的其他基金
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MHC-E 的非典型表位呈递和抗原加工
- 批准号:
10801509 - 财政年份:2023
- 资助金额:
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A Cytomegalovirus-based Vaccine Targeting the Pre-erythrocytic Stage of Malaria
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9982274 - 财政年份:2017
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$ 38.95万 - 项目类别:
A Cytomegalovirus-based Vaccine Targeting the Pre-erythrocytic Stage of Malaria
一种针对疟疾红细胞前阶段的巨细胞病毒疫苗
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9238234 - 财政年份:2017
- 资助金额:
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8423271 - 财政年份:2013
- 资助金额:
$ 38.95万 - 项目类别:
An Effector Memory T Cell-Inducing Subunit Vaccine against Malaria
一种针对疟疾的效应记忆 T 细胞诱导亚单位疫苗
- 批准号:
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- 资助金额:
$ 38.95万 - 项目类别:
MECHANISMS OF IMMUNE VULNERABILITY OF THE ELDERLY TO THE WEST NILE VIRUS
老年人对西尼罗河病毒免疫脆弱的机制
- 批准号:
8357751 - 财政年份:2011
- 资助金额:
$ 38.95万 - 项目类别:
EVASION OF ANTIGEN PRESENTATION BY RHESUS CYTOMEGALOVIRUS
恒河猴巨细胞病毒逃避抗原呈递
- 批准号:
8357750 - 财政年份:2011
- 资助金额:
$ 38.95万 - 项目类别:
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$ 38.95万 - 项目类别:
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- 批准号:
8234067 - 财政年份:2011
- 资助金额:
$ 38.95万 - 项目类别:
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