INTESTINAL CYTOKINE AND T CELL HEMEOSTASIS IN SIV INFECTION

SIV 感染中的肠道细胞因子和 T 细胞止血作用

• 批准号: 8357367
• 负责人: Satya Dandekar
• 金额: $ 14.36万
• 依托单位: UNIVERSITY OF CALIFORNIA AT DAVIS
• 依托单位国家: 美国
• 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: https://reporter.nih.gov/project-details/8357367
• 关键词: California; Chronic; Enteral; Functional disorder; Funding; Grant; HIV; HIV Infections; Health; Immune; Immune System Diseases; Infection; Infection Control; Intestines; Macaca mulatta; Microbe; Modeling; National Center for Research Resources; Patients; Primates; Principal Investigator; Recovery; Research; Research Infrastructure; Resources; SIV; Source; T-Lymphocyte; United States National Institutes of Health; Viral; Virus; cost; cytokine; enteric pathogen; immune activation; insight; microbial; microbial colonization; pathogen; prevent; response; therapeutic target

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 persistence of viral reservoirs and chronic immune activation pose major challenges for achieving complete immune recovery in HIV infected patients, even during long-term therapy. The frontline mucosal immune defenses are crucial in preventing and limiting HIV infection and controlling spread of enteric pathogens and microbial translocation. HIV causes breach in the mucosal defense leading to colonization and microbial translocation of enteric and luminal microbes. This contributes to chronic immune activation and immune dysfunction in HIV infection and supports viral persistence, although mechanisms have not been fully defined. The proposed studies will investigate HIV induced dysfunction in the frontline gut mucosal responses to bacterial pathogens in the SIV infected rhesus macaque model and determine the mechanisms contributing to the inability of the host to control these infections. Gaining insights into the mucosal immune defenses critical in maintaining gut mucosal health will be crucial in identifying therapeutic targets for mucosal protection against the virus and co-infections.

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 而子项目的主要调查员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。 病毒储库的持续存在和慢性免疫激活对实现HIV感染患者的完全免疫恢复构成了重大挑战，即使在长期治疗期间也是如此。前线粘膜免疫防御在预防和限制HIV感染以及控制肠道病原体的传播和微生物易位中至关重要。HIV引起粘膜防御的破坏，导致肠道和管腔微生物的定植和微生物移位。这有助于HIV感染中的慢性免疫激活和免疫功能障碍，并支持病毒持续存在，尽管机制尚未完全确定。 拟议的研究将在SIV感染的恒河猴模型中调查HIV诱导的前线肠道粘膜对细菌病原体反应的功能障碍，并确定导致宿主无法控制这些感染的机制。深入了解对维持肠道粘膜健康至关重要的粘膜免疫防御，对于确定粘膜保护免受病毒和合并感染的治疗靶点至关重要。