PATHOGENESIS OF INTESTINAL DYSFUNCTION IN SIMIAN AIDS

猿猴艾滋病肠功能障碍的发病机制

• 批准号: 7349660
• 负责人: Satya Dandekar
• 金额: $ 15.67万
• 依托单位: UNIVERSITY OF CALIFORNIA AT DAVIS
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-05-01 至 2007-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7349660
• 关键词: PATHOGENESIS; INTESTINAL; DYSFUNCTION; SIMIAN; AIDS

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. Objective: Simian immunodeficiency virus (SIV) and human immunodeficiency virus (HIV) infections lead to rapid depletion of CD4 T cells from gut-associated lymphoid tissue (GALT). Although the administration of antiretroviral therapy (ART) has been shown to increase CD4 T-cell levels in the peripheral blood in both SIV and HIV infections, its efficacy in restoring intestinal mucosal CD4 T cells has not been well investigated. To gain insights into the molecular mechanisms of virally induced disruptions in the mucosal immune system, we have evaluated longitudinal changes in viral burden, T-cell subsets, and mucosal gene expression profiles in SIV-infected rhesus macaques in the absence or presence of ART.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。目的：猿猴免疫缺陷病毒（SIV）和人类免疫缺陷病毒（HIV）感染会导致肠道相关淋巴组织（GALT）中的CD 4 T细胞迅速耗尽。虽然抗逆转录病毒治疗（ART）的管理已被证明可以增加外周血中的CD 4 T细胞水平在SIV和HIV感染，其在恢复肠粘膜CD 4 T细胞的疗效还没有得到很好的研究。为了深入了解病毒诱导的粘膜免疫系统破坏的分子机制，我们评估了在SIV感染的恒河猴中，在ART存在或不存在的情况下，病毒负荷、T细胞亚群和粘膜基因表达谱的纵向变化。