ArticleFrontiers in immunology2026
Lipidomics of HIV/HCV-related liver decompensation: association between plasma lipid depletion and immune dysregulation.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Globally, 15-30% of patients with chronic hepatitis C develop compensated advanced chronic liver disease (cACLD). cACLD may further advance to decompensated ACLD (dACLD), which is associated with higher liver-related mortality, even after successful antiviral treatment. This progression is accelerated by HIV coinfection, yet its underlying molecular mechanisms remain poorly understood. Methods: In this cross-sectional study, we characterized the plasma lipidomic profiles of 58 HIV/HCV-coinfected patients using untargeted liquid chromatography-mass spectrometry. Multivariate (OPLS-DA) and univariate (GLM) statistical models were employed to identify lipid species associated with disease severity. Results: We identified a signature of 28 lipids-predominantly phosphatidylcholines, phosphatidylethanolamines, and triglycerides- that were significantly depleted in patients with dACLD (17.2% of the cohort). This systemic lipid depletion showed relevant correlations with the pro-inflammatory chemokine IP-10 and soluble immune checkpoint proteins. Discussion: Our findings indicate that dACLD in HIV/HCV-coinfection is defined by a profound collapse in plasma lipids. This metabolic failure correlates with markers of inflammation and immune activation, suggesting that lipid dysregulation plays a critical role in the pathogenesis of liver decompensation.
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