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Isolation of Exosomes from the Plasma of HIV-1 Positive Individuals
Published on: January 5, 2016
Stimulant Use, HIV, and Plasma Metabolites Among Men
Emily M Cherenack1, Michaela E Larson2, Kevin Murray3
1Department of Psychiatry and Behavioral Sciences, University of Miami Miller School of Medicine, Miami, FL, USA.
Abstract:
Metabolomics can be used to identify biological targets to mitigate the negative impacts of HIV and stimulant use on neuroimmune and cardiometabolic functioning. However, studies are needed to characterize the plasma metabolome among sexual minority men (SMM) in the context of independent and co-occurring HIV and stimulant use. From 2020 to 2022, we collected plasma samples and assessed biologically confirmed HIV status and stimulant use among 61 community-recruited SMM in Miami, Florida. Cross-sectional bivariate analyses and multivariable regressions correcting for false discovery rate compared 390 mass spectrometry-based plasma metabolites across four HIV/stimulant use groups: (1) living without HIV and no stimulant use (HIV-STIM-), (2) living with HIV and no stimulant use (HIV + STIM-), (3) living without HIV with stimulant use (HIV-STIM +), and (4) living with HIV with stimulant use (HIV + STIM +). Six metabolites showed differences between HIV/stimulant use groups at p < 0.05 in both Kruskal-Wallis tests and linear regressions: choline, tryptophan, two lysophosphatidylcholines, one triacylglyceride, and one dihexosylceramide. After correcting for false discovery rate, in linear regressions controlling for BMI and age, the HIV + STIM + group had lower aspartic acid than the HIV-STIM- group, higher lysophosphatidylcholine a C18:1 than the HIV-STIM + group, and higher triacylglyceride(20:3_34:0) than the HIV-STIM- and HIV + STIM- groups. In SMM, co-occurring stimulant use and HIV were associated with perturbations in certain metabolites. Metabolites such as aspartic acid and lysophosphatidylcholines are potentially involved in immune dysregulation, addiction, energy use, and cardiovascular disease. Trials of interventions to reduce stimulant use could elucidate its causal relationship to metabolites.
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