Association Between Patatin-Like Phospholipase Do-Main-Containing Protein-3 Variant and Cardiovascular Disease Risk

Chia-Hui Yu1, Gwo-Tarng Sheu2, Chien-Feng Li3

  • 1School of Nursing, College of Medicine Chung Shan Medical University Hospital Taichung Taiwan.

Health Science Reports
|February 25, 2026
PubMed

Insights

Single-nucleotide polymorphisms in the PNPLA3 and APOE genes are linked to higher cardiovascular disease (CVD) risk in people with HIV (PLWH) on antiretroviral therapy (ART). Genetic screening may personalize treatment and improve long-term CVD outcomes for PLWH.

Area of Science:

  • Genetics
  • Cardiovascular Medicine
  • Infectious Diseases

Background:

  • People living with HIV (PLWH) on antiretroviral therapy (ART) have an elevated risk of cardiovascular disease (CVD).
  • Genetic factors may influence CVD risk in this population.
  • Understanding these genetic associations is crucial for risk stratification and management.

Purpose of the Study:

  • To investigate the association between specific single-nucleotide polymorphisms (SNPs) in lipoprotein-related genes and CVD risk.
  • To evaluate the impact of these genetic variations on CVD risk scores in PLWH undergoing ART.

Main Methods:

  • Genotyping of four SNPs (ABCB1 rs1045642, APOE rs429358 and rs7412, PNPLA3 rs738409) in 337 PLWH.
  • Calculation of CVD risk using the D:A:D model.
  • Statistical analysis (ANCOVA) to assess associations between SNPs and CVD risk scores, adjusting for covariates.

Main Results:

  • PNPLA3 (rs738409) was significantly associated with higher 10-year CVD risk scores (p=0.03).
  • APOE (rs7412) T allele showed borderline associations with increased CVD risk (p=0.07-0.09).
  • No significant associations were found for ABCB1 or APOE (rs429358).

Conclusions:

  • SNPs in PNPLA3 and APOE may contribute to increased CVD risk in PLWH on ART.
  • Genetic screening could enable personalized treatment strategies for improved long-term CVD outcomes.
  • Further research is warranted to elucidate the mechanisms linking these SNPs to CVD risk.
Abstract

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