Increased carotid intima media thickness is associated with depletion of circulating myeloid dendritic cells in HIV-infected patients on suppressive antiretroviral treatment.

In the present study, plasmacytoid DCs (pDCs) and myeloid DCs (mDCs) were assessed in peripheral blood of a cohort of HIV-infected patients undergoing antiretroviral therapy (ART) and the absolute number of these cells was correlated with carotid intima media thickness (IMT), as surrogate marker for underlying atherosclerosis. We also measured plasma levels of high-sensitivity C-reactive protein (hs-CRP) and tumour necrosis factor (TNF-α), as biomarkers of inflammation. The study population included a total of 36 HIV-infected patients (23 males, 13 females; age range 35–61 years) treated with ART since at least 24 months. The mean duration of HIV infection was 9 ± 2.5 years and the mean duration of therapy with PIs was 4 ± 1.5 years, respectively. All patients were aviremic and the median CD4 was 355 cells/μl. Current smoking was present in 5 patients, while there was no history of angina, myocardial infarction, cardiovascular medication or other atherogenic risk factors. Controls were uninfected adults matched 1:1 to the HIV-infected group by age, gender, race, body mass index (BMI) and traditional cardiovascular risk factors. The carotid IMT (mm) was measured separately in both right and left sides using a colour-doppler ultrasonography. The average value of carotid IMT (mean ± SE) was significantly higher in the HIV-infected patients versus healthy controls (0.80 ± 0.02 vs. 0.601 ± 0.04; p = 0.01). Despite antiretroviral treatment, HIV-infected patients exhibited a significant reduction of both circulating pDCs and mDCs when compared with healthy donors. HIV-infected patients also had significantly higher plasma levels of hs-CRP, while TNF-α was undetectable.In the present study, the depletion of DCs in peripheral blood correlates with accelerated atherosclerosis in HIV-infected patients in spite of a suppressive ART regimen.