Related Experiment Videos
A genome-wide association study of carotid atherosclerosis in HIV-infected men
Sadeep Shrestha1, Marguerite R Irvin, Kent D Taylor
1Department of Epidemiology, School of Public Health, University of Alabama at Birmingham, 1665 University Blvd., Birmingham, AL 35294-0022, USA. sshresth@uab.edu
Insights
Host genetics influence atherosclerosis in HIV patients on HAART. A specific gene variant (RYR3) is linked to common carotid intima-media thickness, a marker for cardiovascular disease.
Area of Science:
- Genetics and Cardiovascular Health
- HIV/AIDS Research
- Medical Diagnostics
Background:
- The genetic factors influencing subclinical atherosclerosis in individuals with HIV receiving highly active antiretroviral therapy (HAART) remain largely uncharacterized.
- Understanding these genetic influences is crucial for managing cardiovascular risk in this population.
Purpose of the Study:
- To investigate the association between host genetics and subclinical atherosclerosis in HIV-infected individuals on HAART.
- To identify specific genetic variations (SNPs and CNVs) linked to carotid intima-media thickness (cIMT) as a measure of atherosclerosis.
Main Methods:
- A genome-wide association study (GWAS) was conducted on 177 HIV-positive Caucasian males from the FRAM Study.
- Carotid intima-media thickness (cIMT) was measured using B-mode ultrasound.
- Single nucleotide polymorphisms (SNPs) and Copy Number Variants (CNVs) were analyzed, with regression analyses performed to assess associations with cIMT, adjusting for relevant covariates.
Main Results:
- Two single nucleotide polymorphisms (SNPs), rs2229116 and rs7177922, within the ryanodine receptor (RYR3) gene on chromosome 15 showed a significant association with common cIMT (P < 1.61 x 10^-7).
- These SNPs are in tight linkage disequilibrium and represent a functional missense polymorphism.
- The RYR gene family is implicated in cardiovascular disease etiology and can be regulated by HIV TAT protein.
Conclusions:
- A functional single nucleotide polymorphism (SNP) in the RYR3 gene is associated with increased common carotid intima-media thickness in HIV-infected individuals undergoing HAART.
- This finding highlights RYR3 as a biologically plausible candidate gene contributing to atherosclerosis in the context of HIV infection and treatment.
Background:
The role of host genetics in the development of subclinical atherosclerosis in the context of HIV-infected persons who are being treated with highly active antiretroviral therapy (HAART) is not well understood.
Methods:
The present genome-wide association study (GWAS) is based on 177 HIV-positive Caucasian males receiving HAART who participated in the Fat Redistribution and Metabolic Change in HIV Infection (FRAM) Study. Common and internal carotid intima-media thicknesses (cIMT) measured by B-mode ultrasound were used as a subclinical measure of atherosclerosis. Single nucleotide polymorphisms (SNPs) were assayed using the Illumina HumanCNV370-quad beadchip. Copy Number Variants (CNV) were inferred using a hidden Markov Model (PennCNV). Regression analyses were used to assess the association of common and internal cIMT with individual SNPs and CNVs, adjusting for age, duration of antiretroviral treatment, and principal components to account for potential population stratification.
Results:
Two SNPs in tight linkage disequilibrium, rs2229116 (a missense, nonsynonymous polymorphism (IIe to Val)) and rs7177922, located in the ryanodine receptor (RYR3) gene on chromosome 15 were significantly associated with common cIMT (P-value < 1.61 x 10). The RYR gene family has been known to play a role in the etiology of cardiovascular disease and has been shown to be regulated by HIV TAT protein.
Conclusion:
These results suggest that in the context of HIV infection and HAART, a functional SNP in a biologically plausible candidate gene, RYR3, is associated with increased common carotid IMT, which is a surrogate for atherosclerosis.
Related Concept Videos
Genome-wide Association Studies-GWAS
GWAS does not require the identification of the target gene involved in...
Atherosclerosis II: Clinical Manifestations and Diagnostic Tests
Amebiasis
Atherosclerosis I: Introduction
Coronary Artery Disease I: Introduction
Atherosclerosis III: Management