T cell senescence predicts subclinical atherosclerosis in HIV-infected patients similarly to traditional cardiovascular risk factors.

The main objective of this study is to evaluate the predictive capacity of T cell activation/senescence in subclinical atherosclerosis (SCA) in a group of HIV-infected patients. So, a cross-sectional analysis was performed on 91 long-term triple-ART therapy HIV-infected patients from an observational and prospective cohort. Carotid Intima Media Thickness (cIMT) was measured. Binary logistic regression was used to evaluate independent variables associated with SCA. Compared to patients without SCA, patients with SCA (60.4%) were older (41.33 ± 9.04 vs. 51.73 ± 8.44 years old, p < 0.001) and showed Framingham risk score (2.63 ± 3.127 vs. 7.66 ± 5.84, p = 0.008), as well as higher numbers of CD4+CD8+ double positive T cells (0.50 ± 0.42% vs. 0.81 ± 0.79%, p = 0.037), CD8+CD28- T cells (41.70 ± 16.96% vs. 50.22 ± 16.15%, p = 0.018), higher expression of CD28 on CD8+CD28+ T cells (1865 ± 789 vs. 2243 ± 917 MFI, P = 0.046). In contrast, they showed lower expression of CD38 on CD19+ B cells (65.38 ± 27.47% vs. 42.67 ± 30.26%, P < 0.001). Logistic multivariable analysis showed that Framingham risk score >10% (OR = 14.84, CI95% 1.63-125; p = 0.016) and numbers of CD8+CD28- T cells (OR = 1.032, CI 95% 1-1.065; p = 0.045) were independent factors associated with SCA. Patients with CD8+CD28- T cells ≥59% compared to those <59% had higher risk of SCA (OR = 4, CI95% 1.19-13.3, p = 0.024). Interestingly, 27.4% of patients with low Framingham risk score had elevated levels of CD8+CD28- T cells. In conclusion, immune senescence represented by accumulation of CD8+CD28- T cells may contribute to improve the predictive capacity of the Framingham risk score, especially when the scores are low and can explain, at least in part, the higher prevalence of SCA observed in long-term ART-treated stable HIV infected patients.