Left Carotid Bulb Intima-Media Thickness Correlates with Age and Specific T lymphocyte Populations in People Living with and without HIV

BackgroundCardiovascular disease (CVD) is a leading cause of mortality worldwide, with carotid atherosclerosis playing a key role in its progression. Carotid intima-media thickness (CIMT) is a well-established biomarker for subclinical atherosclerosis. Emerging evidence suggests that immune dysregulation, particularly T-cell activation and exhaustion, may contribute to vascular pathology. People living with HIV (PLWH) face an elevated risk of CVD, yet the relationship between immune markers and CIMT in this population remains unclear. MethodologyThis cross-sectional study analyzed 100 participants, 70 virologically suppressed PLWH on antiretroviral therapy and 30 HIV-negative controls. Left carotid bulb intima-media thickness (LCBIMT) was measured via ultrasound, and immune markers (CD4+/CD8+ subsets, PD-1+ T-cells, IL-2, IL-17) were assessed. Statistical analyses included Spearman correlations and linear regression models stratified by HIV status to evaluate associations between LCBIMT, age, and lymphocyte subsets. ResultsAge was significantly associated with LCBIMT in both PLWH ({beta}=0.0051, p<0.01) and controls ({beta}=0.0101, p=0.001) groups. CD4+ intermediate % independently predicted LCBIMT in both populations (PLWH: {beta}=0.0110, p=0.02; controls: {beta}=0.0400, p<0.01). Notably, CD4+ naive % showed an unexpected positive association in control participants ({beta}=0.0050, p=0.03). T-cell exhaustion markers (PD-1+) were attenuated after adjustment, while CD8+ intermediate % approached significance in the controls ({beta}=-0.0112, p=0.05). ConclusionHIV infection modifies cardiovascular risk through distinct immune mechanisms, particularly T-cell exhaustion and subset redistribution. These findings suggest immune profiling may aid in early CVD risk stratification and identify potential targets for intervention in high-risk populations, including PLWH.