Background:  The pathogenesis of accelerated atherosclerosis in HIV-infected patients has not well elucidated. Recent lines of evidence indicate that the accumulation of dendritic cells (DC) in the atheroma, especially myeloid DC (mDC), could stimulate both T cell recruitment and activation and may facilitate the release of chemokines, cytokines, and other inflammatory mediators, which are involved in the development and progression of HIV-associated atherosclerosis. We measured in patients on suppressive ART circulating mDC and plasmacytoid DC (pDC) and carotid intima media thickness (IMT), as marker for underlying atherosclerosis.

Methods:  The study population included 36 HIV-infected patients (23 male, 13 female; age range 35 to 61 years) on suppressive ART regimen (median CD4 = 355 cells/µL). Controls were uninfected adults matched 1:1 to the HIV-infected group by age, gender, race, body mass index, and traditional cardiovascular risk factors. pDC and mDC were assessed by using a new whole blood single-platform based on TruCOUNT assay. The carotid IMT was measured separately in both right and left sides (6 predefined segments per side) using a color-doppler ultrasonography. The statistical analysis was done by the Mann-Whitney U test and the Spearman rank correlation test.

Results:  The average value of carotid IMT (mean±SE) was significantly higher in the HIV-infected patients versus healthy controls (0.79 vs 0.6) (p <0.01). Despite effective ART, patients exhibited a significant reduction of circulating pDC and mDC when compared with healthy donors. The median pDC counts were 2078 cells/mL in patients vs 10,179 cells/mL of controls (p <0.001); the median mDC counts were 9453 cells/mL in patients vs 13,265 cells/mL of controls (p <0.04). The lowest levels of DC, especially mDC, were found in patients who had a greater increase in carotid IMT. The analysis of the correlation showed a statistically inverse association between the carotid IMT and the absolute number of mDC (–0.34; p = 0.03) No significant correlation was found between circulating pDC and carotid IMT.

Conclusions:  The present findings suggest that the depletion of DC, especially, mDC in peripheral blood correlates with accelerated atherosclerosis in HIV-infected patients in spite of a suppressive ART regimen. It is possible a recruitment of mDC in the atheroma where these cells contribute to the tissue inflammation and atherosclerotic plaque destabilization.