Association of HIV viral load with monocyte chemoattractant protein-1 and atherosclerosis burden measured by magnetic resonance imaging

Abstract

Background: HIV-infected individuals may be at increased risk for atherosclerosis. Although this is partially attributable to metabolic factors, HIV-associated inflammation may play a role.

Objective: To investigate associations of HIV disease with serum monocyte chemoattractant protein-1/chemokine (C-C motif) ligand 2 (MCP-1/CCL2) levels and atherosclerosis burden.

Design: A cross-sectional analysis.

Methods: : Serum MCP-1/CCL2, fasting lipids, and glucose tolerance were measured in 98 HIV-infected and 79 demographically similar uninfected adults. Eighty-four participants had MRI of the carotid arteries and thoracic aorta to measure atherosclerosis burden. Multivariate analyses were performed using linear regression.

Results: Mean MCP-1/CCL2 levels did not differ between HIV-infected and uninfected participants (P = 0.65). Among HIV-infected participants, after adjusting for age, BMI, and cigarette smoking, HIV-1 viral load was positively associated with MCP-1/CCL2 (P = 0.02). Multivariate analyses adjusting for sex, low-density lipoprotein cholesterol, total cholesterol:high-density lipoprotein cholesterol ratio, cigarette smoking, MCP-1/CCL2, and protease inhibitor use found that HIV infection was associated with greater mean thoracic aorta vessel wall area (VWA, P < 0.01) and vessel wall thickness (VWT, P = 0.03), but not with carotid artery parameters. Compared with being uninfected, having detectable HIV-1 viremia was associated with greater mean thoracic aorta VWA (P < 0.01) and VWT (P = 0.03), whereas being HIV-infected with undetectable viral load was associated with greater thoracic aorta VWA (P = 0.02) but not VWT (P = 0.15). There was an independent positive association of MCP-1/CCL2 with thoracic aorta VWA (P = 0.01) and VWT (P = 0.01).

Conclusion: HIV-1 viral burden is associated with higher serum levels of MCP-1/CCL2 and with atherosclerosis burden, as assessed by thoracic aorta VWA and VWT.

Figure 1

Relationship of monocyte chemoattracted protein-1/chemokine (C-C motif) ligand 2 with HIV-1 viral load and CD4⁺ cell count among HIV-infected participants. This figure shows the relationship of MCP-1/CCL2 with HIV-1 viral load (a) and CD4⁺ cell count (b) among HIV-infected participants. Dashed line represents linear prediction from regression of MCP-1/CCL2 on viral load (P=0.02) and CD4⁺ cell count, respectively (P=0.07), with 95%Cls shown in gray. *HIV-1 viral load was log-transformed to meet criteria for linear regression. CCL2, chemokine (C-C motif) ligand 2; CI, confidence interval; MCP-1, monocyte chemoattractant protein-1.

Figure 2

Relationship of thoracic aorta mean vessel wall area and mean vessel wall thickness with monocyte chemoattractant protein-1/chemokine (C-C motif) ligand 2. The figure shows relationship of thoracic aorta mean VWA (a) and mean VWT (b) with MCP-1/CCL2. Dashed line represents linear prediction from regression on MCP-1/CCL2 of VWA (P=0.01) and VWT (P<0.01), respectively, with 95% CIs shown in gray. CCL2, chemokine (C-C motif) ligand 2; CI, confidence interval; MCP-1, monocyte chemoattractant protein-1; VWA, vessel wall area; VWT, vessel wall thickness.