T CELL ACTIVATION SIGNALS THAT ACTIVATE HIV-1 INFECTION

激活 HIV-1 感染的 T 细胞激活信号

• 批准号: 7605536
• 负责人: Derya Unutmaz
• 金额: $ 10.64万
• 依托单位: VANDERBILT UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-12-01 至 2007-09-16
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7605536
• 关键词: Antigens; Cells; Computer Retrieval of Information on Scientific Projects Database; Funding; Grant; HIV-1; Infection; Institution; Research; Research Personnel; Resources; Rest; Signal Transduction; Source; T-Cell Activation; T-Lymphocyte; United States National Institutes of Health; Viral; cytokine; in vivo; insight

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. The ability of human immunodeficiency virus type-1 (HIV-1) to establish a persistent infection is critically dependent on the cellular signals that regulate HIV-1 replication within target host cells. We propose to identify the activation signals and the signaling mechanisms that are required to render resting T cells susceptible to productive infection. We postulate that the antigenic-independent signals relayed from cytokines and the antigen-presenting cellsactivate bystander resting T cells which in turn is exploited by HIV-1 to infect these target cells. This hypothesis may explain how high viral replication and the T cell turnover is sustained throughout the infection. By pursuing these studies we expect to gain insights into how HIV-1 exploits host's antigen-independent signaling machinery to infect the target cells and the mechanisms of viral spread in vivo.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 人类免疫缺陷病毒类型1（HIV-1）建立持续感染的能力取决于调节靶宿主细胞内HIV-1复制的细胞信号。 我们建议确定激活信号和使静息T细胞易受生产感染所需的信号传导机制。 我们假设从细胞因子和抗原呈递细胞激活旁观者静止的T细胞中传递的抗原独立信号又被HIV-1利用，以感染这些靶细胞。 该假设可以解释在整个感染过程中持续的病毒复制和T细胞更新的高度。 通过追求这些研究，我们希望能够深入了解HIV-1如何利用宿主独立的信号机制感染靶细胞和体内病毒扩散的机制。