Work

Distinct monocyte phenotypes are associated with peri-coronary inflammation in persons with and without HIV and without cardiovascular disease

Year: 2026

Type: article

Abstract: Background and objective Chronic inflammation in persons with (PWH) and without HIV (PWoH) is linked to cardiovascular disease (CVD). The fat attenuation index (FAI), a marker of peri-coronary inflammation, predicts CVD risk. The relationship between FAI and monocyte phenotypes remains unclear. This study aimed to evaluate the relationship between monocyte subsets—classical (CD16dim intermediate/inflammatory monocytes and CD16neg), intermediate, and non-classical— and surface markers of activation and chemokine expression, and FAI in a cohort of PWH and PWoH, and compare relative differences by HIV serostatus. Methods In this cross-sectional of a prospective observational cohort study, 58 virologically suppressed PWH and 16 PWoH without known CVD underwent coronary computed tomography angiography to measure FAI. Peripheral blood monocyte subsets and activation/homing phenotypes were analyzed via flow cytometry. Multivariable regression models assessed correlations between monocyte markers and FAI in the LAD and RCA, with interaction terms testing effects of HIV serostatus. Results Frequency and expression of CD40 were elevated in PWH, while HLA-DR expression was lower across all monocyte subsets compared to PWoH. CD38 + intermediate monocytes were linked to worsened LAD FAI. CD38 + non-classical monocytes were correlated with worsened RCA FAI. CCR2 expression on total classical, and CD16dim, and CD16neg monocytes correlated with worsened RCA and LAD FAI, while CX3CR1 + monocytes and CD40 + subsets correlated with improved RCA FAI in adjusted analyses. Conclusions FAI demonstrates strong correlations with monocyte phenotypes with relationships influenced by HIV serostatus, highlighting activation markers and chemokine receptor profiles as plausible drivers of vascular inflammation and FAI as a tool for detecting early immune-mediated vascular inflammation.

Source: Frontiers in Immunology

DOI: 10.3389/fimmu.2026.1960785