HIV/TB INTERACTION IN THE LUNG

HIV/结核病在肺部的相互作用

• 批准号: 7378234
• 负责人: Michael D. Weiden
• 金额: $ 3.34万
• 依托单位: NEW YORK UNIVERSITY SCHOOL OF MEDICINE
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-04-01 至 2007-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7378234
• 关键词: HIV; TB; INTERACTION; LUNG

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. This study focuses on the transcriptional regulation of HIV-1 replication in alveolar macrophages. Alveolar macrophages from uninflamed lung inhibit HIV-1 replication by expressing a 16kDa inhibitory form of transcription factor C/EBPB (also called NF-IL6 and LIP) producing latent HIV-I infection in the lung. The inflammatory response to tuberculosis reduces C/EBPB expression, derepressing the HIV-1 long terminal repeat and induces another member of the C/EBP transcription factor family which supports high level HIV-1 replication in the lung. The lab was used for the following: DNA isolation, DNA sequencing (automated), ELISA, oligonucleotide synthesis, PCR, recombinant DNA techniques, RNA isolation, Southern analysis, Western analysis, bronchoalveolar lavage processing, EMSA, and use of laminar flow hoods.

该子项目是利用 NIH/NCRR 资助的中心拨款提供的资源的众多研究子项目之一。子项目和研究者 (PI) 可能已从另一个 NIH 来源获得主要资金，因此可以在其他 CRISP 条目中得到体现。列出的机构是中心的机构，不一定是研究者的机构。本研究重点关注肺泡巨噬细胞中 HIV-1 复制的转录调控。来自未发炎肺部的肺泡巨噬细胞通过表达转录因子C/EBPB（也称为NF-IL6和LIP）的16kDa抑制形式来抑制HIV-1复制，从而在肺部产生潜在的HIV-1感染。对结核病的炎症反应会降低 C/EBPB 的表达，解除对 HIV-1 长末端重复序列的抑制，并诱导 C/EBP 转录因子家族的另一个成员，该家族支持肺部中高水平的 HIV-1 复制。该实验室用于以下工作：DNA 分离、DNA 测序（自动）、ELISA、寡核苷酸合成、PCR、重组 DNA 技术、RNA 分离、Southern 分析、Western 分析、支气管肺泡灌洗处理、EMSA 以及层流罩的使用。