Coronary Heart Disease in HIV-Infected Individuals

Vittecoq, D.; Escaut, L.; Merad, Mansouriah; Teicher, Elina; Monsuez, J.-J.; Chironi, Gilles

doi:10.1159/000073181

Cited by 9 publications

(5 citation statements)

References 20 publications

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“…Numerous studies have shown that HIV infection is an independent risk factor for cardiovascular disease [2], [32], [33]; however, the mechanism(s) by which HIV-1 induces cardiovascular disease (CVD) are not well understood and are likely multifactorial. HIVCM are accompanied by traditional cardiovascular risk factors, including endothelial dysfunction, chronic inflammation, lipid disorders, as well as proposed direct HIV-1 infection of the endothelium [34], [35], [36].…”

Section: Discussionmentioning

confidence: 99%

HIV Tat Induces Expression of ICAM-1 in HUVECs: Implications for miR-221/-222 in HIV-Associated Cardiomyopathy

Duan

Yao

et al. 2013

PLoS ONE

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Cardiac involvement is a well-documented complication of human immunodeficiency virus-1 (HIV-1) infection. Previous studies have demonstrated increased adhesion of monocytes to human vascular endothelial cells in HIV-infected individuals. HIV Tat protein, which is the transactivator of transcription (Tat), plays a key role in activating endothelial cells. In the present study, we demonstrated that exposure of HUVECs to HIV Tat protein resulted in induced expression of cell adhesion molecules specifically ICAM-1, leading to increased adhesion of monocytes to the endothelium. This effect of Tat was mediated through activation of mitogen-activated protein kinases and downstream transcription factor NF-κB. Increased expression of ICAM-1 was regulated by microRNA (miRNA) miR-221 and to some extent by miR-222, both of which are known to target ICAM-1. Functional inhibition of the respective miRNAs with anti-miR oligonucleotides resulted in induction of ICAM-1 protein in HUVECs. Furthermore, Tat-stimulated regulation of ICAM-1 via miR-221/-222 involved the NF-kB-dependent pathway. Functional implication and specificity of up-regulated ICAM-1 was confirmed using the ICAM-1 neutralizing antibody in the in vitro cell adhesion assays. These findings were further confirmed in vivo using the HIV transgenic (Tg) rats. These animals not only demonstrated increased expression of ICAM-1 mRNA, with a concomitant reduction in the expression of miR-221 in the aorta and heart, but also had increased expression of the ICAM-1 protein that was predominantly in the endothelial cell layer. Taken together, these findings implicate that Tat-mediated induction of ICAM-1 expression plays a critical role in monocyte adhesion observed in HIV-1-associated cardiomyopathies.

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Section: Discussionmentioning

confidence: 99%

HIV Tat Induces Expression of ICAM-1 in HUVECs: Implications for miR-221/-222 in HIV-Associated Cardiomyopathy

Duan

Yao

et al. 2013

PLoS ONE

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“…There now exists a substantial literature documenting an elevated lifetime prevalence of alcohol use disorders (AUD) among those with an HIV diagnosis and the impact of AUD on the course of HIV, including increased risk for (a) medical comorbidities (e.g., liver, cardiovascular, pulmonary and bone disease) (Friis-Moller et al, 2003; Happel and Nelson, 2005; McComsey et al, 2010; Vittecoq et al, 2003; Weber et al, 2006); (b) poor adherence to medication regimens (Braithwaite et al, 2005; Hinkin et al, 2004); and (c) engagement in risky sexual behavior (Simbayi et al, 2004). What is not yet known, however, is the developmental context that characterizes associations between alcohol consumption and the progression of HIV and related disorders.…”

mentioning

confidence: 99%

Lifetime Drinking Trajectories Among Veterans in Treatment for HIV

Jacob¹,

Blonigen

Upah

et al. 2013

Alcohol Clin Exp Res

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Objective Previous work on the course of drinking across the life course identified four distinct patterns of problem drinking: severe chronic (SC), severe nonchronic (SNC), late onset (LO) and young adult (YA). The purpose of the current study was to determine the generalizability of these findings to a sample of midlife veterans with quite different characteristics from those previously assessed; specifically, veterans in treatment for HIV and veterans in treatment for non-HIV medical issues. Method Participants were drawn from the Veterans Aging Cohort Study (VACS) which included HIV-positive and matched non-HIV participants. As in our earlier studies, the Lifetime Drinking History was used to assess drinking phases, and Latent Growth Mixture Models were used for analyses. Results Similar to previous findings, both the HIV+ and non-HIV groups exhibited four patterns of drinking (SC, SNC, LO, YA). SC drinkers had younger ages of onset for drinking, and longer duration of smoking. SC drinkers also had highest rates of cocaine use. Within the HIV+ subgroup, SC and LO drinkers increased their drinking after their HIV diagnosis. Conclusion This study is the first to examine lifetime drinking patterns among those treated for HIV and provides an excellent starting point for examining finer-grained relationships involving drinking, onset of HIV, and treatment outcomes. Absent from the current study and of particular importance to future work in this area is the need for precise information regarding the temporal relationship between date of HIV diagnosis, onset of treatment and changes in drinking behavior over the life course.

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“…Still, up to 60% of patients receiving HIV PIs develop dyslipidemia, hyperglycemia, and central obesity (4,10,11). These metabolic changes adversely affect several risk factors for atherosclerotic vascular disease (1,21,30).…”

mentioning

confidence: 99%

Ginsenosides block HIV protease inhibitor ritonavir-induced vascular dysfunction of porcine coronary arteries

Chai¹,

Wei²,

Lin³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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Ginsenosides have been shown to have potential benefits on the cardiovascular system through diverse mechanisms, including antioxidative property. The objective of this study was to determine whether ginsenosides could prevent coronary arteries from RTVinduced dysfunction. Porcine coronary artery rings were incubated with RTV and ginsenosides Rb1, Rc, and Re for 24 h. Vasomotor function was recorded by a myograph tension system. In response to the thromboxane A2 analog U-46619, the contraction of the vessel rings was significantly reduced. When cocultured with Rb1, Rc, and Re, the contractility significantly increased. In response to bradykinin at 10 Ϫ5 M, the endothelium-dependent relaxation of vessel rings was significantly reduced by 59% for RTV compared with controls (P Ͻ 0.05). When cocultured with Rb1, Rc, and Re, the relaxation significantly increased 100%, 90%, and 134%, respectively, compared with the RTV-alone groups (P Ͼ 0.05). In response to sodium nitroprusside, RTV significantly reduced vasorelaxation. In addition, the endothelial nitric oxide synthase (eNOS) mRNA levels were significantly reduced by 78% for RTV group (P Ͻ 0.05) by real-time PCR analysis. The eNOS protein levels measured by Western blot analysis and nitrite concentrations measured by Griess assay were also decreased, whereas O 2 Ϫ production by lucigenin-enhanced chemiluminescence was significantly increased in the RTV-treated group. These effects of RTV were effectively blocked by ginsenosides. Thus HIV protease inhibitor RTV significantly impaired the vasomotor function of porcine coronary arteries. This effect may be mediated by the downregulation of eNOS and overproduction of O 2 Ϫ . These results suggest that ginsenosides can effectively block RTV-induced vascular dysfunction. oxidative stress; ginseng root; vasomotor; endothelial nitric oxide; superoxide anion; human immunodeficiency virus

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Coronary Heart Disease in HIV-Infected Individuals

Cited by 9 publications

References 20 publications

HIV Tat Induces Expression of ICAM-1 in HUVECs: Implications for miR-221/-222 in HIV-Associated Cardiomyopathy

HIV Tat Induces Expression of ICAM-1 in HUVECs: Implications for miR-221/-222 in HIV-Associated Cardiomyopathy

Lifetime Drinking Trajectories Among Veterans in Treatment for HIV

Ginsenosides block HIV protease inhibitor ritonavir-induced vascular dysfunction of porcine coronary arteries

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