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Updated: Feb 15, 2026

SILAC Based Proteomic Characterization of Exosomes from HIV-1 Infected Cells
Published on: March 3, 2017
Novel mediators of statin effects on plaque in HIV: a proteomics approach
Chris deFilippi1, Janet Lo2, Robert Christenson3
1Inova Heart and Vascular Institute, Falls Church, Virginia.
Insights
Statin therapy in HIV patients with coronary plaque modulated inflammatory proteins and pathways, offering insights into cardiovascular disease progression. Novel biomarkers may personalize treatments for reducing atherosclerotic coronary vascular disease (ASCVD) in HIV.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Proteomics
Background:
- HIV infection is linked to increased atherosclerotic coronary vascular disease (ASCVD), potentially driven by inflammation.
- Subclinical coronary plaque is common in asymptomatic HIV patients.
- Understanding statin's impact on inflammatory pathways is crucial for managing ASCVD risk in HIV.
Purpose of the Study:
- To investigate how statin therapy affects inflammatory and cardiovascular proteins in HIV patients with subclinical coronary plaque.
- To explore the relationship between these protein changes and alterations in coronary plaque volume.
- To utilize a novel proteomics approach to identify potential biomarkers for ASCVD progression in HIV.
Main Methods:
- A randomized, placebo-controlled trial involving 40 HIV-infected participants.
- Atorvastatin treatment (40 mg/day) versus placebo for 1 year.
- Computed tomography coronary angiography for plaque volume assessment and Olink proteomic panels for protein analysis.
Main Results:
- Six proteins showed significant changes with atorvastatin, many related to innate immunity and inflammation.
- Twenty-six proteins correlated significantly with coronary plaque volume changes over one year.
- Protein changes related to myocardial fibrosis and monocyte chemoattraction were observed with statin treatment and plaque volume, independent of LDL levels.
Conclusions:
- Proteomic analysis reveals statin's influence on novel immune pathways relevant to ASCVD in HIV.
- Biomarker discovery through proteomics can advance precision medicine for ASCVD risk reduction in HIV patients.
- This study provides a foundation for developing targeted therapies to mitigate cardiovascular events in HIV.
Objective:
HIV patients have increased atherosclerotic coronary vascular disease (ASCVD), thought to be mediated through inflammatory mechanisms. We hypothesized that among asymptomatic HIV-infected patients with subclinical coronary plaque, statin therapy would modulate unique inflammatory and cardiovascular proteins in relation to change in subclinical coronary plaque volume. We tested this hypothesis using a novel proteomics approach.
Design:
Forty HIV-infected participants were randomized to atorvastatin (40 mg/day) versus placebo, and underwent computed tomography coronary angiography to quantify plaque volume at baseline and 1 year.
Methods:
We used Olink Cardiovascular III and Cardiometabolic panels based on dual antibody epitope recognition with linked DNA amplification to compare change over time in 184 proteins in treatment versus placebo and in relation to change in coronary plaque volume.
Results:
Six proteins (TFPI, CCL24, NT-Pro BNP, MBL2, LTBR, PCOLCE) changed significantly in the atorvastatin versus placebo group, many in innate immune and other novel inflammatory pathways. Twenty-six proteins changed significantly in relationship to total coronary plaque volume over 1 year. Notably, many of these proteins changed only weakly in relationship to change in low-density lipoprotein (LDL). Overlapping these two broad discovery approaches, proteins involved in myocardial fibrosis/collagen formation and monocyte chemoattraction changed with statin treatment, in relationship to plaque volume, but not LDL.
Conclusion:
This proof-of-concept study employing a proteomic discovery platform offers insight into statin effects on novel immune pathways relevant to ASCVD progression in HIV. Novel biomarker discovery may enhance precision medicine strategies to estimate the efficacy of targeted therapies to reduce ASCVD progression and events in HIV.
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