Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human cytomegalovirus (HCMV) can establish lifelong persistence after primary infection with reactivation occurring as a result of immunosuppression. There is much evidence that molecular interactions between the immune system and the HCMV are responsible for immune escape. HCMV in many cells especially in mononuclear blood cells during latency are frequently the source of transmission and spreading and results in a variety of disorders. In this review some data about acute infection in immunocompetent host (mononucleosis, hepatitis), about intrauterine HCMV infection, about infection and endogenous reinfection in bone marrow and solid organ transplant recipients (pneumonitis) and about HCMV disease in AIDS patients (encephalitis, neuropathy, retinitis, colitis) are investigated. Moreover, HCMV associated vasculitis is described in patients with myocarditis, rheumatoid arthritis or polyradiculopathy. HCMV could play an important role in atherosclerosis. Several types of human malignancy have been linked to HCMV and it has been shown that HCMV ie genes upregulate expression of cellular oncogenes. The diagnosis of HCMV infection is carried out by viremia in cell culture using immediate early antigen staining, by antigenaemia which appears to be an early quantitative and predictive tool, by HCMV DNA detection using hybridization and PCR, and by IgM and IgG antibody evaluation. Two antiviral drugs are used for treatment: ganciclovir and phosphonoformic acid; few resistant clinical isolates have been reported. Specific gammaglobulin activity is discussed. HCMV vaccine is not available.
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PMID:[Current status of human cytomegalovirus disease]. 759 23

Cytomegalovirus (CMV) remains the most important infection affecting heart-transplant recipients. Treatment of clinical disease is with a two to three-week course of intravenous ganciclovir, which is effective in more than 90% of individuals. However, relapsing disease, particularly in those with primary infection, is an increasing problem, occasionally with the development of ganciclovir-resistant infection. In those instances, foscarnet is needed, despite its nephro- and neurotoxicities. Increasingly, in order to prevent relapse, more prolonged oral courses of anti-viral therapy are being added to the standard two to three-week course of intravenous treatment. In the prevention of CMV disease, those at risk of primary disease (donor seropositive, recipient seronegative) should receive prophylaxis; for seropositive transplant patients, preemptive strategies linked to immunosuppression or viremia monitoring are becoming increasingly prevalent. In the future, as new drugs become available, the essential question will be whether chronic allograft injury (i.e., accelerated coronary artery atherosclerosis) can be prevented with an anti-viral strategy.
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PMID:Prevention and treatment of cytomegalovirus disease in heart transplant patients. 1096 65

A link between certain infectious microorganisms and an increased risk of atherosclerotic disease has been suggested. By analyzing the data of subjects who had undergone general health-screening tests, a possible association between carotid atherosclerosis and seropositivity of antibody against hepatitis C virus (HCV) has been previously reported. In the present study, a possible link between carotid atherosclerosis and HCV core protein positivity was assessed, because it is postulated to be a better marker of viremia and thus persistent infection. Of the 1992 enrolled subjects, 496 (25%) had carotid artery plaque, and 25 (1.3%) were positive for HCV core protein. Carotid artery plaque was positive in 480/1967 (24%) and 16/25 (64%) of the core protein-negative and core protein-positive subjects, respectively (p<0.0001 by chi(2) test). Serum concentrations of transaminases were higher in core protein-positive subjects, but albumin concentrations were not significantly different between the 2 groups. Multivariate logistic regression analysis showed that HCV core protein positivity is an independent predictor of carotid plaque with an odds ratio of 5.61 (95% confidence interval 2.06-15.26, p<0.001). These data further support the possible link between persistent HCV infection and carotid atherosclerosis in the subjects without severe liver dysfunction.
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PMID:Association between hepatitis C virus core protein and carotid atherosclerosis. 1252 Jan 47

High levels of L-selectin (CD62L) are a strong indicator of endothelial dysfunction, and atherosclerosis. Atherosclerosis is the leading cause of mortality and morbidity in hemodialysis (HD) patients. Whether HCV infection (highly prevalent in HD patients and also associated with alterations in adhesion molecules) would affect the leukocytic expression and/or the soluble form of L-selectin in hemodialysis patients is unknown. Seventy-two HD patients, HCV-positive (n=48) and HCV-negative (n=24) and 10 normal control were studied. Blood samples were obtained just prior to the start of the dialysis session (predialysis) and at the end of 15 min. of dialysis (intradialysis). The following tests were performed on all patients: HCV-RNA by RT-nested PCR, quantitative determination of sL-selectin by ELISA and neutrophil surface expression of L-selectin (CD62L) by flowcytometry. Both CD62L and sL-selectin were found to be significantly higher in HD patients as compared to normal controls irrespective to HCV. Fifteen minutes after start of the dialysis session both CD62L and absolute neutrophil count decreased significantly [CD62L, p < 0.0001 (HCV-positive), p= 0.03 in (HCV-negative), [neutrophil count, p < 0.0001 each], while sL-selectin showed a significant increase [p = 0.004 (HCV-positive), p = 0.006 (HCV-negative)]. These changes were unrelated to HCV status. A significant increase in CD62L in HCV-positive patients compared to HCV-negative ones in both pre and intradialysis samples was noted (p = 0.007, p = 0.02 respectively). However, no difference was observed in either sL-selectin or absolute neutrophil count between the two groups in the two tested time points. In conclusions, the increased levels of neutrophil-expressed and soluble forms of L-selectin in HD patients, and the intradialysis increase in sL-selectin and decrease in CD62L and neutrophil count are unrelated to HCV viremia. The association between HCV positivity and neutrophil expression of pre andintradialysis L-selectin point to a possible role of HCV that needs further studies.
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PMID:Alterations in neutrophil surface expression of L-selectin (CD62L) and soluble L-selectin (sL-selectin) in hemodialysis patients: relation to HCV. 2030 62

The incidence of HIV is on the rise. With the advent of antiretroviral therapy, the average life expectancy of HIV patients has increased by several decades, but the increasing life expectancy has shifted the spectrum of HIV-associated morbidity and mortality away from opportunistic infections and toward chronic medical conditions. In fact, coronary artery disease has become the leading cause of mortality in patients with HIV. The pathophysiology of atherosclerosis in patients with HIV is very complex, including direct endothelial damage from viremia, a heightened overall state of inflammation from immune activation, higher prevalence and contribution from traditional atherosclerotic risk factors, and direct effects from antiretroviral therapy itself. This review focuses on the patterns, predictors, and pathophysiology of atherosclerotic disease in patients with HIV. In addition, the risks and benefits of evidence-based highly active antiretroviral therapy are critically evaluated.
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PMID:The spectrum of atherosclerotic coronary artery disease in HIV patients. 2042 47

Human cytomegalovirus (HCMV), a double-stranded DNA virus in the herpesvirus family, is a ubiquitous virus that infects greater than 40-60% of the general population and up to 100% within some subpopulations and/or geographic areas (1). HCMV has a complex pathobiology because infection of immunocompetent individuals is rarely associated with severe clinical symptoms and in most cases is simply asymptomatic, whereas HCMV infections can cause a wide range of severe diseases, including mononucleosis, mental retardation, deafness, chorioretinitis, and fatal diseases, such as interstitial pneumonia and disseminated virus infections in immunocom-promised hosts (1). As with other herpesviruses, HCMV is thought to establish latent or persistent infections. Reactivation of this infection is frequently encountered during pregnancy and in organ transplant and acquired immune deficiency syndrome (AIDS) patients (1). In addition, HCMV has been implicated as a co-etiological agent in cervical cancer (2) and has been found associated with a wide range of other tumors (1). More recently, HCMV has also been shown to be epidemiologically linked to restenosis (3-5) and atherosclerosis (5,6). The severity of these HCMV-associated diseases warrants an accurate ability to detect and diagnose persons with HCMV, especially because of the clinical availability of the anti-HCMV agents, ganciclovir and foscarnet, which have been used successfully to treat patients with HCMV viremia.
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PMID:Immunological methods for the detection of human cytomegalovirus. 2134 Sep 49

HIV-1 elite controllers spontaneously maintain suppressed levels of viremia, but exhibit significant immune activation. We investigated coronary atherosclerosis by coronary computed tomography angiography (CTA) in elite controllers, nonelite controller, chronically HIV-1 infected, antiretroviral therapy (ART)-treated patients with undetectable viral load ('chronic HIV'), and HIV-negative controls. Prevalence of atherosclerosis (78 vs. 42%, P < 0.05) and markers of immune activation were increased in elite controllers compared with HIV-negative controls. sCD163, a monocyte activation marker, was increased in elite controllers compared with chronic HIV-1 (P < 0.05) and compared with HIV-negative controls (P < 0.05). These data suggest a significant degree of coronary atherosclerosis and monocyte activation among elite controllers.
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PMID:Increased coronary atherosclerosis and immune activation in HIV-1 elite controllers. 2303 11

Several lines of evidence suggest the involvement of infectious agents in the pathogenesis of atherosclerosis. Furthermore, a correlation between infection-driven inflammatory burden and acute manifestation of coronary artery disease has been hypothesized. The aim of this work was to assess whether human herpesvirus (HHV)-6 and HHV-8, two DNA viruses with a distinct tropism for endothelium and lymphocytes, may be associated with coronary instability. An age- and gender-matched cross-sectional study was undertaken in 70 patients with testing of plasma HHV-6 and HHV-8 DNA load in different cardiovascular clinical settings: 29 patients with acute myocardial infarction, 21 patients with stable coronary artery disease, and 20 patients without coronary and carotid artery atherosclerosis subjected to cardiac valve replacement. In all patients, HHV-6 and HHV-8 plasma DNA was tested by using highly sensitive, calibrated quantitative real-time PCR assays which employ a synthetic DNA calibrator to adjust for DNA extraction and amplification efficiency. HHV-8 viremia was undetectable in all three groups. HHV-6 viremia was detected in a substantial fraction of the samples examined (18.6%) without significant differences among the three groups (ST segment elevation myocardial infarction: 17.2%; stable coronary artery disease: 14.3%; patients without coronary and carotid artery atherosclerosis: 25%). Furthermore, no significant differences in plasma HHV-6 load were observed amongst the three groups of patients. These findings indicate that coronary instability is not associated specifically with active HHV-6 or HHV-8 infection. However, an unusually high rate of active HHV-6 infection was documented among patients without atherosclerosis admitted to hospital with cardiac disease.
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PMID:Molecular study of human herpesvirus 6 and 8 involvement in coronary atherosclerosis and coronary instability. 2308 May 3

The development of efficient combined antiretroviral therapies has lengthened the mean life span of the population affected with human immunodeficiency virus (HIV) transforming this terminal infection to a chronic yet manageable disease. Nonetheless, patients with HIV--treatment naive or not--exhibit larger risks for coronary artery disease than the noninfected population. Moreover, coronary atherosclerosis/arteriosclerosis may be the most prevalent condition in the HIV-infected population that is being accentuated by the effects of viral agents and the antiretroviral drugs, especially protease inhibitors. Nonetheless, generalized metabolic dysfunctions and premature senescence are often attributed to the viremia caused by the HIV infection directly and primarily. Therefore, a multifactorial approach is to be considered when attempting to explain the strong correlation between HIV and coronary artery disease, including co-opportunistic viremias and vitamin D insufficiency/deficiency.
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PMID:Coronary Artery Disease in the Human Immunodeficiency Virus Seropositive Population. 2379 58

The study of HIV-infected "controllers" who are able to maintain low levels of plasma HIV RNA in the absence of antiretroviral therapy (ART) may provide insights for HIV cure and vaccine strategies. Despite maintaining very low levels of plasma viremia, controllers have elevated immune activation and accelerated atherosclerosis. However, the degree to which low-level replication contributes to these phenomena is not known. Sixteen asymptomatic controllers were prospectively treated with ART for 24 weeks. Controllers had a statistically significant decrease in ultrasensitive plasma and rectal HIV RNA levels with ART. Markers of T cell activation/dysfunction in blood and gut mucosa also decreased substantially with ART. Similar reductions were observed in the subset of "elite" controllers with pre-ART plasma HIV RNA levels below conventional assays (<40 copies/mL). These data confirm that HIV replication persists in controllers and contributes to a chronic inflammatory state. ART should be considered for these individuals (ClinicalTrials.gov NCT01025427).
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PMID:Prospective antiretroviral treatment of asymptomatic, HIV-1 infected controllers. 2457 Oct 10


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