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Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
Published on: October 17, 2017
Monocytes in HIV associated atherosclerosis: A review of pathogenesis and clinical implications
Peyman Eini1, Pooya Eini2, Sara Pourhemmati3
1Infectious Disease Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
Insights
People with HIV (PLWH) face amplified atherosclerosis risk due to immune activation and HIV-specific factors. Comprehensive care integrating ART, lifestyle changes, and targeted therapies is crucial to reduce cardiovascular disease risk.
Area of Science:
- Cardiovascular Science
- Immunology
- Infectious Disease
Background:
- Atherosclerosis is a leading cause of death globally, with heightened risk in people living with HIV (PLWH) due to persistent immune activation and traditional cardiovascular risk factors.
- HIV-specific mechanisms, including viral proteins and gut microbial translocation, exacerbate chronic inflammation and monocyte dysfunction, accelerating atherosclerosis in PLWH.
- While antiretroviral therapy (ART) has improved longevity, it doesn't fully resolve immune activation, leaving monocyte-driven inflammation central to ongoing atherosclerosis progression.
Purpose of the Study:
- To review the amplified atherosclerosis risk in PLWH.
- To discuss the impact of HIV-specific mechanisms and ART on cardiovascular disease (CVD) risk.
- To explore current and future therapeutic strategies for mitigating CVD in PLWH.
Main Methods:
- Literature review of studies on atherosclerosis in PLWH.
- Analysis of HIV-specific inflammatory pathways and their role in atherogenesis.
- Evaluation of imaging techniques for subclinical atherosclerosis detection (e.g., CIMT, CAC scoring).
- Assessment of adjunctive therapies, including statins and anti-inflammatory agents.
Main Results:
- PLWH exhibit accelerated atherosclerosis due to persistent immune activation, HIV proteins, and gut microbial translocation.
- Protease inhibitor-based ART regimens are linked to metabolic disturbances, worsening dyslipidemia and insulin resistance.
- Subclinical atherosclerosis is prevalent in PLWH, detectable via imaging techniques.
- Statins and anti-inflammatory agents show potential in reducing inflammation and CVD risk.
Conclusions:
- Comprehensive management of PLWH must integrate ART optimization with lifestyle interventions, lipid management, and novel therapies targeting immune dysfunction.
- Targeted strategies addressing monocyte activation, chronic inflammation, and gut microbial translocation are essential.
- Further research is needed to refine biomarkers, personalize CVD risk assessment, and develop innovative treatments to reduce cardiovascular morbidity and mortality in PLWH.
Abstract:
Atherosclerosis, a chronic inflammatory disease of arterial walls, remains a leading cause of global mortality, with ischemic heart disease (IHD) and stroke as primary contributors. In people living with HIV (PLWH), this risk is amplified due to persistent immune activation and conventional cardiovascular risk factors such as hypertension and dyslipidemia. HIV-specific mechanisms, including viral proteins, gut microbial translocation, and chronic inflammation, drive monocyte dysfunction, foam cell formation, and vascular damage, contributing to accelerated atherogenesis. Antiretroviral therapy (ART) has significantly improved the life expectancy of PLWH, transforming HIV into a chronic condition. However, ART does not fully normalize immune activation, particularly monocyte-driven inflammation, which remains central to atherosclerosis progression. Protease inhibitor (PI)-based ART regimens are associated with metabolic disturbances, exacerbating dyslipidemia and insulin resistance, further increasing cardiovascular disease (CVD) risk. Imaging techniques, such as carotid intima-media thickness (CIMT) and coronary artery calcium (CAC) scoring, reveal subclinical atherosclerosis in this population. Adjunctive therapies like statins and anti-inflammatory agents, including interleukin (IL)-1β antagonists, show promise in mitigating inflammation and CVD risk. Targeted strategies addressing monocyte activation, chronic inflammation, and gut microbial translocation are critical. Comprehensive care for PLWH requires integrating ART optimization with lifestyle interventions, lipid-lowering therapies, and novel treatments targeting immune dysfunction. Future research should refine biomarkers for early atherosclerosis detection, tailor CVD risk assessments, and explore therapeutic innovations to reduce cardiovascular morbidity and mortality in PLWH.
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