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

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。尽管宿主防御的表型后果尚不清楚，但人类基因组中的片段重复选择性地富集了与免疫有关的基因。我们推测人类染色体17q上的一个片段复制热点可能与对HIV-1等传染病的免疫有关，因为它包含两个CC趋化因子基因，CC趋化因子配体3样1 （CCL3L1）和CCL4L1。我们选择HIV感染作为模型系统来验证我们的假设，即引起宿主防御基因剂量效应的片段复制与体内表型效应相关。为了验证这一假设，我们确定了来自57个种群的1,064名人类和83只黑猩猩中含有趋化因子基因的片段重复的分布