Hiv tat protein causes endothelial dysfunction in porcine coronary arteries

Paladugu, Ramesh; Fu, Weiping; Conklin, Brian S.; Lin, Peter H.; Lumsden, Alan B.; Yao, Qizhi; Chen, Changyi

doi:10.1016/s0741-5214(03)00770-5

Cited by 72 publications

(64 citation statements)

References 39 publications

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“…32 As a consequence, Tat protein causes endothelial dysfunction. 33 The death of CD4 T lymphocytes caused by HIV results in an increase in shed membrane particles from these cells. 34 Shed membrane particles from T lymphocytes induce endothelial dysfunction, expressed as a reduction in nitric oxide and prostacyclin-induced vasodilation.…”

Section: Endothelial Dysfunction and Hiv Infectionmentioning

confidence: 99%

What a Cardiologist Needs to Know About Patients With Human Immunodeficiency Virus Infection

Hsue

Waters

2005

Circulation

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Patient case: A 48-year-old man with human immunodeficiency virus (HIV) infection developed chronic chest pain that started after a bout of pneumonia. He has hypertension and has smoked cigarettes in the past. His current medications include Kaletra and Combivir. His total cholesterol was 331 mg/L, his HDL cholesterol was 27 mg/L, his triglycerides were 935 mg/L, and his LDL cholesterol could not be calculated. How should this patient be evaluated and managed?

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Section: Endothelial Dysfunction and Hiv Infectionmentioning

confidence: 99%

What a Cardiologist Needs to Know About Patients With Human Immunodeficiency Virus Infection

Hsue

Waters

2005

Circulation

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“…Also, in-vitro studies of endothelial function have implicated HIV as potentially having direct and indirect effects on the endothelium, including direct infection and/or activation of endothelial cells by HIV, vascular injury as a result of chronic inflammation and immune activation, or dysregulation of the nitric oxide synthase system [32][33][34][35]. Both tat and gp120 proteins of the HIV virion may activate endothelial cells, resulting in increased expression of specific adhesion molecules (i.e., ICAM-1, E-selectin) that may contribute to endothelial dysfunction or a prothrombotic state [33][34][35]. Thus, it is possible that subjects in the current study had overall low cardiovascular risk due to good control of HIV viremia and adequate restoration of immunity.…”

Section: Discussionmentioning

confidence: 99%

Insulin resistance predicts endothelial dysfunction and cardiovascular risk in HIV-infected persons on long-term highly active antiretroviral therapy

Mondy

Fuentes²,

Önen³

et al. 2008

Aids

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Objective-Cardiovascular disease risk among persons with HIV is likely multifactorial, thus testing a variety of available noninvasive vascular ultrasound and other surrogate tests may yield differing results. To address this issue, we assessed multiple metabolic and clinical predictors of endothelial function and carotid intima-media thickness in HIV-infected subjects and compared results with HIV-negative controls.Design-Prospective, cross-sectional study of 50 HIV-infected, healthy adults on stable highly active antiretroviral therapy matched to 50 HIV-negative controls by age, sex, race, and body mass index.Methods-Flow-mediated vasodilation of the brachial artery, carotid intima-media thickness, dual energy X-ray absorptiometry (HIV-infected subjects), and fasting insulin, lipids, and oral glucose tolerance tests were performed. Results were compared between HIV-infected and control groups.Results-Fifty percent of subjects were African-American with 34% women. Among HIVinfected, mean CD4 cell count was 547 cells/ µl; 90% had HIV RNA less than 50 copies/ml. There were no significant differences between HIV-infected and control subjects with regard to brachial artery flow-mediated vasodilation or carotid intima-media thickness. In multivariate analyses of the HIV cohort, independent predictors of endothelial dysfunction (lower flow-mediated vasodilation) were increasing insulin resistance, greater alcohol consumption, and higher baseline brachial artery diameter (P < 0.05); predictors of increased carotid intima-media thickness were hypertension, higher trunk/limb fat ratio, and insulin resistance (P < 0.05).Conclusion-In this HIV cohort on modern highly active antiretroviral therapy with well controlled HIV, there were no significant differences with regard to preclinical markers of cardiovascular disease. Insulin resistance was a strong predictor of impaired brachial artery flowmediated vasodilation and increased carotid intima-media thickness, and may be an important cardiovascular disease risk factor in the HIV population.

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“…Then excess NO reacts with oxygen radicals to produce peroxynitrite, which then causes oxidative damage to the vascular endothelium, and decreased flow mediated dilation (Jacobson et al, 2004;Torre, 2006). The HIV transactivator of viral replication (tat) protein has been found to significantly decrease eNOS mRNA and thus impair vasorelaxation in porcine coronary arteries (Paladugu et al, 2003). The HIV surface protein gp120 (envelope glycoprotein) also stimulates NO production in activated macrophages, and directly activates endothelial cells resulting in increased adhesion of leukocytes to the endothelium, causing endothelial damage (Mu et al, 2007).…”

Section: Pathophysiology Of Hiv-associated Cardiovascular Diseasementioning

confidence: 99%

Human Immunodeficiency Virus infection and cardiovascular disease

2017

Int. J. Curr. Res. Med. Sci.

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The human immunodeficiency virus (HIV) is a retrovirus belonging to the family of lentiviruses. Retroviruses are so named because they reverse the normal flow of genetic information. In all cellular organisms the genetic material is DNA. Retroviruses use their RNA and host DNA to make viral DNA. Infection with HIV causes severe damage to the immune system leading to Acquired Immune Deficiency Syndrome (AIDS). Individuals infected with HIV show both cellular and humoral (antibody) immune responses to the virus, but these responses are unable to prevent the ultimate progression of disease in the great majority of infected individuals. Depletion of CD4 lymphocytes is the hallmark of HIV infection, and predicts an individual's risk for infection with opportunistic pathogens as well as other complications of HIV disease. There is a great association of HIV and cardiovascular disease due to a higher prevalence of underlying traditional cardiovascular risk factors that are mostly host dependent. Most of the HIV drugs increase the chances of cardiovascular diseases in the patients especially protease inhibitors. Chronic inflammation, hypercoagulability and platelet activation all contribute to endothelial dysfunction, and are a probable link between HIV and cardiovascular disease.

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Hiv tat protein causes endothelial dysfunction in porcine coronary arteries

Cited by 72 publications

References 39 publications

What a Cardiologist Needs to Know About Patients With Human Immunodeficiency Virus Infection

What a Cardiologist Needs to Know About Patients With Human Immunodeficiency Virus Infection

Insulin resistance predicts endothelial dysfunction and cardiovascular risk in HIV-infected persons on long-term highly active antiretroviral therapy

Human Immunodeficiency Virus infection and cardiovascular disease

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