Format

Send to

Choose Destination
HIV Clin Trials. 2016 May;17(3):114-22. doi: 10.1080/15284336.2016.1162386. Epub 2016 Apr 4.

Non-classical monocytes predict progression of carotid artery bifurcation intima-media thickness in HIV-infected individuals on stable antiretroviral therapy.

Author information

1
a Hawaii Center for AIDS, John A. Burns School of Medicine , University of Hawaii , Honolulu , HI , USA.
2
b The Queen's Medical Center , Honolulu , HI , USA.
3
c University of Southern California Atherosclerosis Research Unit , CA , USA.
4
d Straub Medical Center , Honolulu , HI , USA.
5
e Blood Systems Research Institute , San Francisco , CA , USA.
6
f Department of Laboratory Medicine , University of California , San Francisco , CA , USA.
7
g Department of Medicine , University of California , San Francisco , CA , USA.

Abstract

BACKGROUND:

Inflammation may contribute to cardiovascular disease (CVD) among antiretrovirally suppressed HIV-infected individuals. We assessed relationships of monocyte, CD8 T-cell activation and plasma biomarkers to changes in carotid artery intima-media thickness (CIMT).

METHODS:

Longitudinal study of HIV-infected subjects ≥40 years and on stable antiretroviral therapy (ART) ≥3 months. Peripheral blood mononuclear cells were immunophenotyped by multiparameteric flow cytometry to quantify classical (CD14(++)CD16(-)), intermediate (CD14(++)CD16(+)), non-classical (CD14(low/+)CD16(++)) and transitional (CD14(+)CD16(-)) monocyte subsets and activated (CD38(+)HLA-DR(+)) CD8(+) T-cells at baseline. Plasma biomarkers were assessed by multiplex Luminex assay. High-resolution B-mode ultrasounds of right carotid arteries were obtained. Changes in CIMT over two years at the right common carotid artery (CIMTCCA) and right bifurcation (CIMTBIF) were outcome variables.

RESULTS:

We studied 50 subjects: 84% male, median age 49 (Q1, Q3; 46, 56) years, median CD4 count 461 (317, 578) cells/mm(3), and with HIV RNA ≤ 50 copies/mL in 84%. Change in CIMTBIF correlated with log values of baseline absolute count of non-classical monocytes (r = 0.37, p = 0.020), and with MCP-1 (r = 0.42, p = 0.0024) and TNF-α (r = 0.30, p = 0.036) levels. In multivariable linear regression, only non-classical monocytes and MCP-1 predicted the change in CIMTBIF, independent of Framingham Risk Score and baseline CIMTBIF. No correlation was noted between CD8 T-cell activation and CIMTBIF change. Monocyte subsets, CD8 T-cell activation, and biomarker concentrations were not correlated with changes in CIMTCCA.

CONCLUSIONS:

Our findings highlight the role of non-classical monocytes and MCP-1 in the progression of CIMTBIF in HIV-infected individuals on stable ART independent of traditional cardio-metabolic risk factors.

KEYWORDS:

Biomarkers; CIMT; HIV; Monocytes

PMID:
27125366
PMCID:
PMC4892178
DOI:
10.1080/15284336.2016.1162386
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Taylor & Francis Icon for PubMed Central
Loading ...
Support Center