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Published on: August 31, 2014
Functionally-informed fine-mapping identifies genetic variants linking increased CHD1L expression and HIV restriction
Riley H Tough1,2, Paul J McLaren3,4,
1Sexually Transmitted and Bloodborne Infections Surveillance and Molecular Epidemiology, Sexually Transmitted and Bloodborne Infections Division at the JC Wilt Infectious Diseases Research Centre, National Microbiology Laboratories, Public Health Agency of Canada, Winnipeg, MB, R3E 3L5, Canada.
Genetic variants near the CHD1L gene influence Human Immunodeficiency Virus Type 1 (HIV) viral load. This study reveals how these variants affect CHD1L gene expression and HIV replication in monocytes, offering insights into HIV restriction.
Area of Science:
- Genetics
- Virology
- Immunology
Background:
- Human Immunodeficiency Virus Type 1 (HIV) set-point viral load predicts disease progression and transmission risk.
- Genome-wide association studies identified a chromosome 1 region linked to decreased HIV viral load in individuals of African ancestries.
- The CHD1L gene, located near this region, showed enhanced HIV replication upon knockout in myeloid cells.
Purpose of the Study:
- To investigate the association between HIV set-point viral load (spVL) associated variants and CHD1L gene expression.
- To identify specific variants influencing HIV spVL and their regulatory impact on CHD1L.
- To explore the relationship between genetically regulated CHD1L expression and HIV restriction in monocytes.
Main Methods:
- Applied a heuristic fine-mapping approach to prioritize variants associated with HIV spVL.
- Assessed the impact of prioritized variants on CHD1L gene regulation using public sequencing data.
- Tested the correlation between imputed CHD1L expression in monocytes and HIV spVL.
Main Results:
- Identified specific genetic variants influencing CHD1L regulation and HIV spVL.
- Demonstrated a link between genetically regulated CHD1L expression and HIV restriction in monocytes.
- Characterized the role of CHD1L in controlling HIV replication.
Conclusions:
- Genetically regulated CHD1L expression plays a role in controlling HIV viral load.
- Findings expand understanding of CHD1L's mechanism in HIV restriction within monocytes.
- This research provides genetic insights into HIV pathogenesis and potential therapeutic targets.
