Abstract
IntroductionSuboptimal ART adherence, despite HIV viral suppression, has been associated with chronic residual inflammation. Whether this association extends to individuals who initiate ART during early HIV infection remains unknown, which was the objective of this study.MethodsPlasma levels of interleukin‐6 (IL‐6), high‐sensitivity C‐reactive protein, serum amyloid A protein (SAA), IL‐27, soluble intercellular adhesion molecule‐1, soluble vascular adhesion molecule‐1, D‐dimer and the CD4+/CD8+ T‐cell ratio, were analysed at baseline and eight months after ART initiation in treatment‐naïve participants with HIV and CD4+ T‐cells >500 cells/mm3 enrolled in the immediate arm of START. Adherence was assessed by seven‐day self‐report. Multivariable linear regression was utilized to analyse the association between ART adherence and each biomarker at the eight‐month visit in participants who achieved virologic suppression (<50 copies/mL).ResultsWe evaluated 1627 participants (422 female) who achieved virologic suppression at the eight‐month visit in the period between 2009 and 2013. Median (IQR) CD4+ T‐cell count before ART was 651 (585, 769) cells/mm3. Incomplete adherence was reported in 109 (7%) participants at the eight month visit. After adjusting for covariates, plasma IL‐6 was 1.12 (95% CI, 1.00 to 1.26; p = 0.047) fold higher in participants reporting incomplete versus 100% adherence. A similar association for SAA was observed in an exploratory analysis (1.29 (95% CI 1.04 to 1.60); p = 0.02). No significant differences in other biomarkers were observed.ConclusionsIncomplete ART adherence was associated with higher IL‐6 levels in individuals who achieved virologic suppression early after ART initiation in START. A potential similar association for SAA requires confirmation. These findings suggest a role for identifying strategies to maximize ART adherence even during virologic suppression. ClinicalTrials.gov number: NCT00867048.
Highlights
Suboptimal antiretroviral therapy (ART) adherence, despite HIV viral suppression, has been associated with chronic residual inflammation
People living with HIV (PLHIV) continue to benefit from antiretroviral therapy (ART) by preventing progression to AIDS [1,2] and transmission to their partners [3]
Even in the setting of durable and sustained virologic suppression, PLHIV exhibit a phenotype of enhanced residual inflammation, immune activation and coagulopathy [4] that is predictive of serious non-AIDS events, including cardiovascular disease, non-AIDS-related malignancies and all-cause mortality
Summary
Suboptimal ART adherence, despite HIV viral suppression, has been associated with chronic residual inflammation. Recent studies have demonstrated that suboptimal (i.e. less than 100%) ART adherence could be a significant contributing factor to the chronic residual inflammation, coagulopathy and immune activation observed in PLHIV even if it is sufficient to achieve and sustain plasma viral suppression through routinely available assays [18,19,20]. These associations have been identified in PLHIV who are on chronic ART [18,20] and who have recently initiated ART [19]. Whether variations in ART adherence, beyond virologic suppression, are associated with heightened chronic residual inflammation, immune activation and coagulopathy in early treated HIV infection remains unknown
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