HOST GENETIC DETERMINANTS OF HIV PATHOGENESIS

这个子项目是利用由NIH/NCRR资助的中心拨款提供的资源的许多研究子项目之一。子项目和调查员(PI)可能从另一个NIH来源获得了主要资金，因此可能会出现在其他CRISE条目中。列出的机构是针对中心的，而不一定是针对调查员的机构。人类基因组中的节段性复制选择性地丰富了参与免疫的基因，尽管宿主防御的表型后果尚不清楚。我们推测，人类染色体17q上的节段性复制热点可能与对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感染作为一个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的表型效应有关。为了验证这一假设，我们确定了来自57个种群的1064名人类和83只黑猩猩中含有趋化因子基因的节段性复制的分布

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