Monocytes from men living with HIV exhibit heightened atherogenic potential despite long-term viral suppression with antiretroviral therapy

Thomas A. Angelovich, Janine M. Trevillyan, Jennifer F. Hoy, Michelle E. Wong, Paul A. Agius, Anna C. Hearps, Anthony Jaworowski

Research output: Contribution to journalArticleResearchpeer-review

3 Citations (Scopus)


Objective:People living with HIV have an increased risk of cardiovascular disease (CVD) despite effective antiretroviral therapy (ART). Monocytes play a key role in the early stages of atherosclerosis-driven CVD by forming lipid-laden foam cells within artery walls. HIV infection potentiates foam cell formation ex vivo, but the mechanisms contributing to this are not known.Methods:We investigated the atherosclerosis-promoting potential of monocytes from 39 virologically suppressed men living with HIV (MLHIV) on ART and no evidence of CVD, and 25 HIV-uninfected controls of comparable age, sex, smoking status and CVD risk.Results:Despite absence of clinical atherosclerosis in both MLHIV and uninfected cohorts (evidenced by a carotid intima-media thickness of 0.6mm for both groups; P=0.254), monocytes from MLHIV showed increased potential to form atherosclerosis-promoting foam cells compared with controls in an ex-vivo assay (36.6% vs. 27.6%, respectively, P=0.003). Consistent with observations of persistent inflammation and immune/endothelial activation in ART-treated HIV infection, levels of soluble tumour necrosis factor receptor II, CXCL10 and soluble VCAM-1 were elevated in MLHIV (P≤0.005 for all), but were not significantly associated with foam cell formation. Foam cell formation was associated with an impaired ability of monocytes to undergo reverse transmigration, and a reduced ability to efflux cholesterol ex vivo (P<0.05 for both). Importantly, foam cell formation declined significantly with duration of viral suppression (P=0.004).Conclusion:These findings highlight the persistence of HIV-related changes to the atherogenic potential of monocytes despite long-term viral suppression, and provide insights into mechanisms potentially driving increased CVD in ART-treated HIV infection.

Original languageEnglish
Pages (from-to)513-518
Number of pages6
Issue number4
Publication statusPublished - 15 Mar 2020


  • atherosclerosis
  • foam cell
  • HIV
  • monocyte
  • oxidized HDL

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