GBV-C viremia was significantly associated with prolonged survival among HIV-positive men 5 to 6 years after HIV seroconversion, but not at 12 to 18 months, and the loss of GBV-C RNA by 5 to 6 years after HIV seroconversion was associated with the poorest prognosis. Understanding the mechanisms of interaction between GBV-C and HIV may provide insight into the progression of HIV disease.
Many predictors of lower QOL are alterable risk factors that can be effectively targeted for interventions to maximize patients' QOL. With appropriate treatment and management of HIV disease and depression, clinicians can help improve the QOL of their patients. Through modification of individual risk behaviors, HIV-infected individuals can enhance their own QOL with support from clinicians and the community. In addition, active social support can also be an effective way to improve mental health of the infected persons.
(See the editorial commentary by Feinstein and Lloyd-Jones on pages 1343-5.)Background. Monocytes and monocyte-derived macrophages promote atherosclerosis through increased inflammation and vascular remodeling. This may be especially true in chronic human immunodeficiency virus (HIV) infection.Methods. We examined 778 women (74% HIV + ) in the Women's Interagency HIV Study and 503 men (65% HIV + ) in the Multicenter AIDS Cohort Study who underwent repeated B-mode carotid artery ultrasound imaging in 2004-2013. We assessed baseline associations of the serum macrophage inflammation markers soluble (s)CD163, sCD14, galectin-3 (Gal-3), and Gal-3 binding protein (Gal-3BP) with carotid plaque formation (focal intima-media thickness >1.5 mm) over 7 years.Results. Marker levels were higher in HIV + persons versus HIV -persons. Presence of focal plaque increased over time: from 8% to 15% in women, and 24% to 34% in men. After adjustment for demographic, behavioral, and cardiometabolic factors, and CRP and interleukin-6, each standard deviation increase in sCD14 was associated with increased plaque formation (risk ratio [RR] 1.24, 95% confidence interval [CI] 1.07-1.43). This pattern was consistentby sex. sCD163 was associated with plaque formation in virally suppressed HIV + men (RR 1.52, 95% CI 1.04-2.22); Gal-3BP and Gal-3 were not associated with increased plaque.Conclusions. sCD14 and sCD163 may play important roles in atherogenesis among HIV + persons.
The QOL of participants has been dynamic over the HIV disease course. HIV infection deteriorated physical but not mental QOL. In this group, although the PHS following HAART has remained lower than that prior to infection, HAART has enhanced mental health functioning.
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