HIV-related cardiovascular disease: any role for high-density lipoproteins?

Abstract

The introduction of antiretroviral therapy (ART) has improved the life expectancy of patients infected with human immunodeficiency virus (HIV). However, this population is at an increased risk for non-communicable diseases, including atherosclerotic cardiovascular disease (CVD). Both ART and viral infection may be potential contributors to the pathophysiology of HIV-related CVD. The mechanisms behind this remain unclear but it is critical to delineate early biomarkers of cardiovascular risk in the HIV population. In this review, we postulate that potential biomarkers could include alterations to high-density lipoprotein (HDL). Indeed, recent data suggest that HIV and ART may induce structural changes of HDL, thus resulting in shifts in HDL subclass distribution and HDL functionality

Alterations in Th17 Cells and Non-Classical Monocytes as a Signature of Subclinical Coronary Artery Atherosclerosis during ART-Treated HIV-1 Infection

“…In addition, plasma markers of intestinal damage (FABP2), systemic inflammation (sCD14), and chemokines involved in cell trafficking (CCL20, MIF, and CX3CL1) were significantly higher in HIV + compared to HIV − participants. This is indicative that ART does not restore gut barrier function or counteract systemic immune activation in PLWH, thus explaining the increased CVD risk associated with HIV-1 infection relative to the general population [7,8,10,[13][14][15].…”

“…Indeed, PLWH tend to present clinical signs of CVD approximately 10 years earlier compared to the general population [11]. In addition to traditional CVD risk factors (e.g., smoking, hypertension, dyslipidemia, diabetes, insulin resistance, and/or sedentary life-style) [12] and mental health disorders with an impact on CVD risk, HIV-specific mechanisms (e.g., HIV-mediated metabolic alterations due to long-term administration of ART) contribute to the premature occurrence of CVD in ART-treated PLWH [7,8,10,[13][14][15]. In addition, the persistence of HIV reservoirs during ART is associated with impaired intestinal mucosal barrier function, microbial translocation, immune dysfunction, and chronic inflammation, which, together with CMV and other co-infections, contribute to an increased CVD risk in this group [16][17][18][19][20].…”

The effects of ART on the dynamics of lipid profiles in Chinese Han HIV-infected patients: comparison between NRTI/NNRTI and NRTI/INSTI

“…Atherogenic dyslipidemia, including low HDL-C and high TC, were main cardiovascular risk factors in HIV-infected patients ( 6 , 15 , 16 ). Recent findings have indicated that decreased levels of HDL-C were directly associated with increased CVD risk, and that providing screening and treatment services for ART patients with high cholesterol would reduce the overall CVD risk ( 21–23 ). Therefore, recommendations regarding the use of INSTIs regimens should balance their benefits with their potential metabolic harm and CVD risks.…”

A Blood Immunological Signature of Subclinical Coronary Artery Atherosclerosis in People Living with HIV-1 Receiving Antiretroviral Therapy

“…In addition, plasma markers of intestinal damage (FABP2), systemic inflammation (sCD14), and chemokines involved in cell trafficking (CCL20, MIF, and CX3CL1) were significantly higher in HIV + compared to HIVparticipants. This is indicative that ART does not restore gut barrier functions, nor counteracts systemic immune activation in PLWH, thus explaining an increased CVD risk associated with HIV-1 infection relative to the general population [7,8,10,[13][14][15].…”

“…Indeed, PLWH tend to present clinical signs of CVD approximately 10 years earlier compared to general population [11]. In addition to traditional CVD risk factors (e.g., smoking, hypertension, dyslipidemia, diabetes, insulin resistance, and/or sedentary life-style) [12] and mental health disorders with an impact on CVD risk, HIV-specific mechanism (e.g., HIV-mediated metabolic alterations due to long-term administration of ART) contribute to the premature occurrence of CVD in ART-treated PLWH [7,8,10,[13][14][15]. In addition, the persistence of HIV reservoirs during ART is associated with impaired intestinal mucosal barrier functions, microbial translocation, and immune dysfunction, and chronic inflammation, which, together with CMV and other coinfections, contribute to an increased CVD risk in this group [16][17][18][19][20].…”