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.

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