Asymptomatic Atherosclerosis in HIV-positive Patients: A Case-control Ultrasound Study

Constans, J.; Marchand, J.M.; Conri, C.; Peuchant, Evelyne; Seigneur, M.; Rispal, P; Lasseur, Catherine; Pellegrin, Jean‐Luc; Leng, B

doi:10.3109/07853899509019256

Cited by 51 publications

(29 citation statements)

References 6 publications

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“…Indeed, a large number of lymphocytes and monocytes are seen in the brain tissues of HIV-1-infected patients who suffer from AIDS dementia complex (Nottet, 1999;Nottet et al, 1996). HIV-1 infection is also associated with an increased frequency of vascular complications such as atherosclerosis (Constans et al, 1995;Tabib et al, 2000). Up-regulation of endothelial ICAM-1 could promote monocyte infiltration into the vascular wall, contributing to vascular lesion formation.…”

Section: Hiv-1 Gp120 Increases Icam-1 Expressionmentioning

confidence: 99%

Section: B Oth Human Immunodeficiency Virus (Hiv)-positivementioning

confidence: 99%

“…Indeed, HIV-1-infected leukocytes can transmigrate into the central nervous system and cause encephalopathy (Nottet, 1999). Endothelial cell dysfunction and leukocyte infiltration may also be attributable to the increased frequency of vascular complications such as atherosclerosis in HIV-1-infected patients (Constans et al, 1995;Tabib et al, 2000).Several factors may contribute to the increased levels of cell adhesion molecules in HIV-1 infection. Elevated levels of proinflammatory cytokines such as TNF-␣ and IL-1␤ have been detected in serum of AIDS patients and in macrophages isolated from HIV-1-infected individuals (Butl et al, 1993;Lahdevirta et al, 1988).…”

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confidence: 99%

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HIV-1 Envelope Glycoprotein 120 Increases Intercellular Adhesion Molecule-1 Expression by Human Endothelial Cells

Ren

Yao

Chen

2002

Laboratory Investigation

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SUMMARY:Human immunodeficiency virus type 1 (HIV-1) infection is often associated with central nervous system damage and vascular complications. However, the mechanisms of this association are largely unknown. We examined the effect of HIV-1 envelope glycoprotein 120 (gp120) on cell adhesion molecule expression by endothelial cells. We found, for the first time, that both soluble and membrane-bound gp120 could significantly increase the expression of human endothelial intercellular adhesion molecule-1 (ICAM-1) at both mRNA and protein levels, but not vascular cell adhesion molecule-1 and E-selectin. The specificity of gp120-mediated response was demonstrated by blocking experiments using a specific monoclonal antibody against gp120, which successfully abolished the gp120-mediated increase of ICAM-1 expression. Furthermore, there was a significant increase of human monocytic cell line THP-1 adherence onto the gp120-treated endothelial monolayers. This increased cell adhesion was effectively blocked by either anti-gp120 or anti-ICAM antibodies. These findings suggest that HIV-1 gp120-mediated endothelial ICAM-1 expression could be one of the important mechanisms of HIV-1 pathogenesis. (Lab Invest 2002, 82:245-255). B oth human immunodeficiency virus (HIV)-positiveand acquired immune deficiency syndrome (AIDS) patients often have significantly increased levels of circulating cell adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) (Greenwood et al, 1998; Seigneur et al, 1997). Serum ICAM-1 levels correlate well with AIDS progression in HIV type 1 (HIV-1)-infected patients (Galea et al, 1997). Endothelial cells and leukocytes from these patients exhibit a significant increase of such adhesion molecules (Pillet et al, 1999;Zietz et al, 1996). HIV-1 particles also incorporate many cell adhesion molecules (Guo and Hildreth, 1995). HIV-associated ICAM-1 is biologically active and can enhance virus infectivity (Fortin et al, 1997) and virus-induced syncytium formation (Gruber et al, 1991). ICAM-1-bearing viruses are less susceptible to neutralization by anti-envelope glycoprotein 120 (gp120) monoclonal antibodies than the same virus produced in cells expressing no ICAM-1 (Sawyer et al, 1994). HIV-1 replication in monocytes/macrophages is significantly enhanced by interaction with endothelial cells through cell adhesion molecules (Gilles et al, 1995). In addition, alterations in expression of cell adhesion molecules by leukocytes and endothelial cells can increase leukocyte migration into the tissues, which may result in certain organ damage. Indeed, HIV-1-infected leukocytes can transmigrate into the central nervous system and cause encephalopathy (Nottet, 1999). Endothelial cell dysfunction and leukocyte infiltration may also be attributable to the increased frequency of vascular complications such as atherosclerosis in HIV-1-infected patients (Constans et al, 1995;Tabib et al, 2000).Several factors may contribute to the increased levels of cell adhesion mole...

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Section: Hiv-1 Gp120 Increases Icam-1 Expressionmentioning

confidence: 99%

Section: B Oth Human Immunodeficiency Virus (Hiv)-positivementioning

confidence: 99%

mentioning

confidence: 99%

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HIV-1 Envelope Glycoprotein 120 Increases Intercellular Adhesion Molecule-1 Expression by Human Endothelial Cells

Ren

Yao

Chen

2002

Laboratory Investigation

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“…Moreover, an increased incidence of cardiovascular events has been reported in AIDS patients (9), and recent reports suggest a correlation between intensity of immunodeficiency and presence of atherosclerotic plaques (10). Lastly, a significant decrease in CD4 cells has been described in the blood of atomic bomb survivors, and an increased incidence of myocardial infarction in this population has been found to be associated with a lower proportion of CD4 cells (11).…”

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confidence: 99%

CD4 Cell Lymphopenia and Atherosclerosis in Renal Transplant Recipients

Ducloux

Challier²,

Saas³

et al. 2003

Journal of the American Society of Nephrology

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Abstract. Several animal studies suggest that T cell-mediated immunodeficiency may play a role in the progression of atherosclerosis. This study examined the association between lymphocyte subsets and atherosclerotic events in renal transplant recipients. A total of 302 consecutive renal transplant recipients were enrolled in this prospective study. Peripheral blood lymphocyte subsets were quantified and analyzed with respect to other known cardiovascular risk factors. The patients were followed for a mean duration of 23.5 Ϯ 4.5 mo. Mean CD4, CD8, and CD19 cell levels were 511 Ϯ 290/mm 3 , 553 Ϯ 596/mm 3 , and 66 Ϯ 62/mm 3 , respectively. CD4 levels were positively related to transplant duration (r ϭ 0.32; P ϭ 0.02) and inversely related to age (r ϭ 0.35; P ϭ 0.01). Twenty-five atherosclerotic events (AE) occurred in 25 patients (8.3%). CD4 levels were lower in patients who experienced CVE (288 Ϯ 170/mm 3 versus 531 Ϯ 290/mm 3 ; P Ͻ 0.0001). Cox regression analysis showed that patients in the three upper quartiles of CD4 cell count had a decreased risk of CVE compared with those in the lowest quartile. There was a linear increase in risk of CVE with decreasing CD4 cell count (P Ͻ 0.0001). A CD4 cell count in the highest quartile (Ͼ663/mm 3 ) divided the risk of CVE by 10 as compared with the lowest quartile. In conclusion, CD4 lymphocytopenia is an independent risk factor for the development of cardiovascular complications in renal transplant recipients, suggesting that impaired immune response promotes accelerated atherogenesis in this population.Stable renal transplant recipients (RTR) have disproportionately high rates of arteriosclerotic outcomes (1). An increased prevalence of traditional cardiovascular risk factors cannot fully explain this increased incidence of CVE in the transplant population (2), and our group has recently emphasized the role of nontraditional cardiovascular risk factors, such as hyperhomocysteinemia (3). A recent study from the USRDS registry showed an increased cardiovascular mortality in RTR having received polyclonal antilymphocyte globulins (4), suggesting either that intense immunosuppression may accelerate native atherosclerosis or that polyclonal antithymocyte globulins exerts specific longterm detrimental effects on the course of atherosclerosis. Nevertheless, interpretation of this finding is challenged by the fact that the atherosclerotic lesion contains large number of immune cells, particularly macrophages and T cells. Furthermore, atherosclerosis is associated with systemic immune responses, including inflammation.On the other hand, several animal studies have shown that immunosuppression may accelerate native atherosclerosis (5-8).Moreover, an increased incidence of cardiovascular events has been reported in AIDS patients (9), and recent reports suggest a correlation between intensity of immunodeficiency and presence of atherosclerotic plaques (10). Lastly, a significant decrease in CD4 cells has been described in the blood of atomic bomb survivors, and an increased inci...

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“…Endothelial function at the brachial artery provides a surrogate measure of the coronary circulation and a correlate of the severity of coronary artery disease [25,87,88]. Accordingly, abnormal brachial artery endothelial function has been associated with a wide spectrum of cardiovascular risk factors, including dyslipidaemia, smoking, diabetes and hypertension [88][89][90][91]. Endothelial dysfunction is considered the key step in the development of atherosclerosis and it is known to be an early predictor of future cardiovascular events in patients without and with known cardiovascular disease [92][93][94][95].…”

Section: Available Methods For Assessment Of Endothelial Functionmentioning

confidence: 99%

Endothelial function and cardiovascular diseases in HIV infected patient

Andrade¹,

Cotter²

2006

Braz J Infect Dis

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The HIV epidemic has dramatically changed the paradigm for the development of drug therapy in the last 15 years. The goal is now not only to provide an effective reduction of plasma viremia , but also to reconstitute the immune deficiency due to the progression of the disease. Significant problems with the metabolism of sugars and lipids lead to the appearance of well-documented disorders such as insulin resistance, abnormalities in lipid metabolism and lipodystrophy in those patients on prolonged therapy with antiretrovirals. The question of whether or not HAART-associated lipid disorders contribute to the premature development of coronary artery disease is of major importance for the HIV community. Endothelial injury is associated with disease-related biochemical abnormalities that are implicated in HIV pathogenesis. The exploration of endothelial function began in the early 1980s at the start of the epidemic. The study of endothelial function in HIV infection and its modifications by HAART is an exciting new field in clinical research; in this review the available information on cardiovascular diseases associated with HIV infection and its treatment are discussed.

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Asymptomatic Atherosclerosis in HIV-positive Patients: A Case-control Ultrasound Study

Cited by 51 publications

References 6 publications

HIV-1 Envelope Glycoprotein 120 Increases Intercellular Adhesion Molecule-1 Expression by Human Endothelial Cells

HIV-1 Envelope Glycoprotein 120 Increases Intercellular Adhesion Molecule-1 Expression by Human Endothelial Cells

CD4 Cell Lymphopenia and Atherosclerosis in Renal Transplant Recipients

Endothelial function and cardiovascular diseases in HIV infected patient

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