Alcohol and dietary factors associate with gut integrity and inflammation in HIV-infected adults.

OBJECTIVES: HIV-infected adults have heightened monocyte activation and inflammation, at least partially as a consequence of altered gut integrity. The role of dietary factors in microbial translocation and inflammation and their downstream effect on markers of cardiovascular disease (CVD) have not been explored. Our purpose was to describe the longitudinal dietary patterns of HIV-infected adults, and to examine the relationship between dietary intake, gut integrity, inflammation and subclinical markers of CVD in HIV-infected adults. METHODS: We conducted a secondary analysis of 147 HIV-infected participants in a 96-week randomized clinical trial of rosuvastatin as primary CVD prevention. Dietary intake was assessed using dietary recall; plasma gut integrity, monocyte activation and inflammation markers were measured using an enzyme-linked immunosorbent assay (ELISA); and CVD risk was assessed using carotid ultrasound and the coronary artery calcium score. Linear mixed models were used to analyse longitudinally measured biomarkers. RESULTS: The median age was 45 years and 78% of patients were male. At baseline, participants consumed a mean (standard deviation) of 108 (70) g of fat daily, 19 (15.6) g of fibre, 266 (186) g of carbohydrates and 15.6 (5.9) g of protein; 45% of the sample consumed alcohol. Over time, alcohol consumption was associated with several markers of gut integrity and inflammation (all P < 0.05). CONCLUSIONS: HIV-infected adults in a contemporary, high-resource setting have poor dietary patterns. Alcohol use was associated with worse gut integrity and increased inflammation, while other aspects of diet (fibre, carbohydrates and fat) were not. These data add to growing evidence illustrating the need for a better understanding of the effect of lifestyle factors on comorbidities in HIV-infected adults.

Markers of inflammation and CD8 T-cell activation, but not monocyte activation, are associated with subclinical carotid artery disease in HIV-infected individuals.

OBJECTIVES: The aim of the study was to explore the relationships between lymphocyte and monocyte activation, inflammation, and subclinical vascular disease among HIV-1-infected patients on antiretroviral therapy (ART). METHODS: Baseline mean common carotid artery (CCA) intima-media thickness (IMT) and carotid plaque (IMT > 1.5 cm) were evaluated in the first 60 subjects enrolled in the Stopping Atherosclerosis and Treating Unhealthy Bone with Rosuvastatin in HIV (SATURN-HIV) trial. All subjects were adults on stable ART with evidence of heightened T-cell activation (CD8(+)CD38(+)HLA-DR(+) ≥ 19%) or increased inflammation (high-sensitivity C-reactive protein ≥ 2 mg/L). All had fasting low-density lipoprotein (LDL) cholesterol ≤ 130 mg/dL. RESULTS: Seventy-eight per cent of patients were men and 65% were African-American. Median (interquartile range) age and CD4 count were 47 (43, 52) years and 648 (511, 857) cells/µL, respectively. All had HIV-1 RNA < 400 HIV-1 RNA copies/mL. Mean CCA-IMT was correlated with log-transformed CD8(+)CD38(+)HLA-DR(+) percentage (r = 0.326; P = 0.043), and concentrations of interleukin-6 (r = 0.283; P = 0.028), soluble vascular cell adhesion molecule (sVCAM; r = 0.434; P = 0.004), tumour necrosis factor-α receptor-I (TNFR-I; r = 0.591; P < 0.0001) and fibrinogen (r = 0.257; P = 0.047). After adjustment for traditional cardiovascular disease (CVD) risk factors, the association with TNFR-I (P = 0.007) and fibrinogen (P = 0.033) remained significant. Subjects with plaque (n = 22; 37%) were older [mean (standard deviation) 51 (7.7) vs. 43 (9.4) years, respectively; P = 0.002], and had a higher CD8(+)CD38(+)HLA-DR(+) percentage [median (interquartile range) 31% (24, 41%) vs. 23% (20, 29%), respectively; P = 0.046] and a higher sVCAM concentration [mean (standard deviation) 737 (159) vs. 592 (160) ng/mL, respectively; P = 0.008] compared with those without plaque. Pro-inflammatory monocyte subsets and serum markers of monocyte activation (soluble CD163 and soluble CD14) were not associated with CCA-IMT or plaque. CONCLUSIONS: Participants in SATURN-HIV have a high level of inflammation and immune activation that is associated with subclinical vascular disease despite low serum LDL cholesterol.