HOST GENETIC DETERMINANTS OF HIV PATHOGENESIS

HIV发病的宿主遗传决定因素

• 批准号: 7349823
• 负责人: Sunil K Ahuja
• 金额: $ 2.01万
• 依托单位: TEXAS BIOMEDICAL RESEARCH INSTITUTE
• 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/7349823
• 关键词: HOST; GENETIC; DETERMINANTS; HIV; PATHOGENESIS

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. Segmental duplications in the human genome are selectively enriched for genes involved in immunity, although the phenotypic consequences for host defense are unknown. We surmised that a hot-spot for segmental duplications on human chromosome 17q might be relevant to immunity against infectious diseases such as HIV-1, since it encompasses two CC chemokine genes, CC chemokine ligand 3-like 1 (CCL3L1) and CCL4L1. We selected HIV infection as a model system in which to test our hypothesis that segmental duplications causing dosage effects of host defense genes are associated with phenotypic effects in vivo. To test this hypothesis, we determined the distribution of chemokine gene-containing segmental duplications in 1,064 humans from 57 populations and 83 chimp

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。列出的机构适用于该中心，这不一定是调查员的机构。尽管未知宿主防御的表型后果，但人类基因组中的节段重复有选择地富集与免疫的基因。我们推测，针对人类17q的节段性重复的热点可能与针对感染性疾病（例如HIV-1）的免疫力有关，因为它涵盖了两个CC趋化因子基因，即CC趋化因子配体3类样1（CCL3L1）和CCL4L1。我们选择了HIV感染作为一种模型系统，在其中测试了我们的假设，即导致宿主防御基因的剂量效应的节段性重复与体内的表型效应有关。为了检验这一假设，我们确定了来自57个人群和83个黑猩猩的1,064人中含趋化因子基因的分段重复的分布