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Isolation of Exosomes from the Plasma of HIV-1 Positive Individuals
Published on: January 5, 2016
Persistent inflammatory activation in people living with HIV. Involvement in atherosclerosis
Francisco Illanes-Álvarez1,2,3, Denisse Márquez-Ruiz1,2,3, Sara Cuesta-Sancho1,2,4
1Servicio de Medicina Interna, Hospital Universitario Puerta del Mar, Cádiz, Spain.
Insights
People living with HIV (PLWH) show higher inflammatory and platelet markers, linked to atherosclerosis. Cardiovascular risk factors and inflammation independently impact subclinical atherosclerosis in PLWH.
Area of Science:
- Cardiovascular Health
- Infectious Diseases
- Immunology
Background:
- Increased atherosclerosis prevalence observed in people living with HIV (PLWH).
- HIV infection is associated with chronic inflammation and immune dysregulation.
- Subclinical atherosclerosis poses a significant health risk for PLWH.
Purpose of the Study:
- To analyze inflammatory, immune, endothelial, platelet, and coagulation parameters in PLWH.
- To investigate the relationship between these markers and subclinical atherosclerosis.
- To identify factors influencing atherosclerosis development in PLWH.
Main Methods:
- Study included 120 PLWH and 30 HIV-uninfected controls.
- Measured serum levels of inflammatory markers (IL-6, sCD163, hs-CRP), NET-derived parameters, activated T lymphocytes, endothelial markers (E-selectin, VCAM-1), platelet markers (P-selectin, PF4), and coagulation markers (D-dimer).
- Assessed subclinical atherosclerosis using carotid Doppler ultrasound in a subset of participants.
Main Results:
- PLWH exhibited elevated levels of IL-6, sCD163, anti-nucleosome antibodies, activated T lymphocytes, platelet factor 4, and D-dimer compared to controls.
- PLWH with carotid atherosclerotic lesions had higher cardiovascular risk scores (REGICOR, ASCVD) and IL-6 levels.
- REGICOR score and IL-6 serum levels were identified as independent factors associated with atherosclerosis.
Conclusions:
- Long-term viral load control in PLWH is associated with increased inflammatory, immune, platelet, and coagulation markers.
- Subclinical atherosclerosis in PLWH is independently influenced by traditional cardiovascular risk factors and heightened inflammatory activation.
Background:
An increased prevalence of atherosclerosis has been observed in people living with HIV (PLWH). This study aimed to analyze levels of inflammatory, immune, endothelial, platelet, and coagulation parameters, as well as their relationship with subclinical atherosclerosis.
Methods:
A total of 120 PLWH with chronic infection and undetectable HIV load, along with 30 age- and sex-matched controls (HIV-uninfected individuals), were selected. Serum levels of proinflammatory molecules, including interleukin 6 (IL-6), soluble CD163, and high-sensitivity C-reactive protein, were measured. Additionally, neutrophil extracellular traps (NET)-derived parameters (anti-nucleosome antibody titers and myeloperoxidase concentrations), activated T lymphocytes, endothelial (E-selectin, vascular cell adhesion molecule 1), platelet (P-selectin, Platelet factor 4) and coagulation (D-dimer) markers were assessed. Cardiovascular risk factors were evaluated using the REGICOR and ASCVD risk estimators. In a subset of 61 individuals (18 controls and 43 PLWH), subclinical atherosclerosis was assessed by carotid Doppler ultrasound.
Results:
Levels of IL-6, sCD163, anti-nucleosome antibodies, and activated T lymphocytes were elevated in PLWH compared to controls. Likewise, serum levels of platelet factor 4 and D-dimer were higher in PLWH. Those PLWH with carotid atherosclerotic lesions exhibited higher REGICOR and ASCVD scores, as well as elevated IL-6 concentrations, compared to those PLWH without carotid atherosclerotic lesions. Multivariable analysis identified the REGICOR score and IL-6 serum levels as independent factors associated with atherosclerosis.
Conclusion:
People living with HIV with long-term viral load control exhibit increased levels of inflammatory, immune, platelet and coagulation markers. Subclinical atherosclerosis in this population is independently influenced by both classic cardiovascular risk factors and inflammatory activation.
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