HOST GENETIC DETERMINANTS OF HIV PATHOGENESIS

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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