Key result
Nadir CD4+ <200 and CD4/CD8 ≥1.0 in HIV linked to ~245% higher odds of severe cIMT.
Why the study?
HIV infection can promote persistent immune activation and endothelial dysfunction contributing to atherosclerosis, but the association of immune dysregulation markers with carotid intima-media thickness severity needed evaluation in people living with HIV.
Is immune dysregulation (low CD4+ nadir and CD4/CD8 ratio) associated with increased carotid intima-media thickness in people living with HIV?
Cross-Sectional (n=1,148)
Yes
Is immune dysregulation (low CD4+ nadir and CD4/CD8 ratio) associated with increased carotid intima-media thickness in people living with HIV?
In people living with HIV, a lower CD4+ nadir combined with immune dysregulation is associated with greater severity of subclinical atherosclerosis as measured by carotid intima-media thickness.
Supports consideration of CD4 nadir in CV risk assessment for PLWH; extends evidence linking immune dysregulation with subclinical atherosclerosis.[[1]](https://pubmed.ncbi.nlm.nih.gov/41902291/)[[2]](https://www.mdpi.
HIV infection can promote persistent immune activation and endothelial dysfunction, contributing to atherosclerosis. Carotid intima–media thickness (cIMT) is an established marker of subclinical atherosclerosis. We evaluated the association between cIMT severity and two routinely available markers of immune dysregulation (CD4/CD8 ratio and nadir CD4+ cell count) in people living with HIV (PLWH). We conducted an Italian multicenter cross-sectional study including 1148 PLWH who underwent carotid color Doppler ultrasound. We classified cIMT as ≤0.9, 1.0–1.4, or >1.4 mm and analyzed these categories using multinomial logistic regression, reporting adjusted odds ratios (aORs) with 95% confidence intervals (CIs). We adjusted models for age, sex, BMI, HIV acquisition risk factor, hypertension, diabetes, dyslipidemia/statin use, triglycerides, integrase inhibitor use, and ART duration. cIMT was ≤0.9 mm in 615 (53.6%) participants, 1.0–1.4 mm in 379 (33.0%), and >1.4 mm in 154 (13.4%). Using nadir CD4+ ≥ 200 cells/µL and CD4/CD8 ≥ 1.0 as reference, PLWH with nadir CD4+ < 200 and CD4/CD8 ≥ 1.0 had higher odds of cIMT 1.0–1.4 mm (aOR 1.66, 95% CI 1.02–2.69) and >1.4 mm (aOR 3.45, 95% CI 1.68–7.07). In conclusion, CD4+ nadir and this combined pattern were associated with greater cIMT severity, supporting a role for immune dysregulation in subclinical atherosclerosis.
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Ceccarelli et al. (2026) conducted a cross-sectional in HIV infection (n=1,148). Nadir CD4+ < 200 cells/µL and CD4/CD8 ≥ 1.0 vs. Nadir CD4+ ≥ 200 cells/µL and CD4/CD8 ≥ 1.0 was evaluated on Carotid intima-media thickness (cIMT) >1.4 mm (aOR 3.45, 95% CI 1.68-7.07). A nadir CD4+ < 200 cells/µL combined with CD4/CD8 ≥ 1.0 in people living with HIV was associated with higher odds of severe carotid intima-media thickness >1.4 mm (aOR 3.45; 95% CI 1.68–7.07).
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