MR SPECTROSCOPY IN THE SIV INFECTED MACAQUE MODEL OF NEUROAIDS

感染 SIV 的神经艾滋病猕猴模型中的 MR 光谱

• 批准号: 7958297
• 负责人: RAMON GILBERTO GONZALEZ
• 金额: $ 11.19万
• 依托单位: HARVARD MEDICAL SCHOOL
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-05-01 至 2010-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7958297
• 关键词: AIDS Dementia Complex; AIDS neuropathy; Animals; Bone Marrow; CD8-Positive T-Lymphocytes; Cerebrum; Computer Retrieval of Information on Scientific Projects Database; Event; Experimental Designs; Funding; Goals; Grant; HIV; HIV Infections; Infection; Injury; Institution; Lead; Macaca; Macaca mulatta; Magnetic Resonance; Magnetic Resonance Spectroscopy; Measurement; Modeling; Monkeys; Neuronal Injury; Neurons; New England; Pathogenesis; Pathway interactions; Phagocytes; Primates; Recovery; Research; Research Personnel; Resources; SIV; SIV encephalitis; Series; Source; Testing; United States National Institutes of Health; base; macrophage; monocyte; theories; trafficking

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. Our goal is to elucidate the pathways that lead to cerebral injury by HIV infection. Neuroinvasion occurs soon after infection and up to 30 percent of those infected with HIV develop AIDS dementia complex (ADC). A leading theory for the pathogenesis of neuroAIDS is that a specific bone marrow derived blood monocyte is virally infected and activated, then traffics into the CNS where it becomes a perivascular macrophage and sets off a cascade of events that result in neuronal injury. We seek to understand the dynamics of monocytic phagocyte (MP) trafficking, MP turnover in the CNS and neuronal recovery through an experimental design that tests a series of specific hypotheses derived from the central theory. This will be accomplished by combining immunological, immunohistochemical, pathological, and magnetic resonance spectroscopic measurements of SIV-infected rhesus macaque monkeys. Towards this end we are utilizing the SIV-infected, CD8+ T lymphocyte depleted macaque model (SIV+/CD8-) which typically results in a reliable accelerated model of neuroAIDS; 95 percent of persistently (long-term) depleted animals demonstrate histopathological signs of SIV encephalitis.

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 我们的目标是阐明HIV感染导致脑损伤的途径。神经侵袭在感染后不久就会发生，高达30%的艾滋病毒感染者会患上艾滋病痴呆综合症(ADC)。神经艾滋病发病机制的一个主要理论是，特定的骨髓来源的血液单核细胞被病毒感染和激活，然后进入中枢神经系统，在那里它成为血管周围的巨噬细胞，并引发一系列导致神经元损伤的事件。我们试图通过实验设计来测试一系列源自中心理论的特定假设，以了解单核细胞吞噬细胞(MP)在中枢神经系统的转运、MP周转和神经元恢复的动力学。这将通过结合免疫学、免疫组织化学、病理学和核磁共振光谱测量SIV感染的恒河猴来实现。为此，我们正在利用SIV感染的CD8+T淋巴细胞耗尽猕猴模型(SIV+/CD8-)，这通常会导致可靠的加速神经艾滋病模型；95%的持续(长期)耗尽的动物显示出SIV脑炎的组织病理学迹象。