Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Over the last few years emerging evidence indicate the involvement of herpes viruses in the pathogenesis of several medical complications in transplanted patients. Herpes viruses are transmitted via inter-human contact and cause a primary infection, which commonly fails to give clinical signs and may persist even for years in a latent state in healthy subjects. In transplanted patients, herpes viruses may be transmitted through the transplanted organ or may be reactivated because of the use of powerful immunosuppressive drugs. Moreover, the persistence of immunosuppression greatly favours the clinical expression and severity of virus infection. Thus, herpes viruses seem to be involved in both acute and chronic deterioration of graft function, in the pathogenesis of post-transplant lymphoproliferative disorders and Kaposi sarcoma, and even in vessel atherosclerosis. This review will focus on relevant clinical aspects of herpes-virus infection, namely cytomegalovirus, EBV, herpes simplex 1 and 2, varicella zoster virus, HHV-6, HHV-7 and HHV-8, in kidney transplanted patients.
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PMID:[Herpetic viruses and renal transplantation]. 1219

Although evidence is far from being conclusive, several studies have suggested that infections could trigger rejection in different transplant settings. In this review we examine the evidence linking cytomegalovirus (CMV), adenovirus, enterovirus, parvovirus, and herpes simplex virus infections to the vasculopathy leading to cardiac allograft rejection, the association between CMV and chronic kidney, lung, and liver graft rejection, and the association of human herpesvirus 6 reactivation with CMV-related disease in kidney and liver transplant recipients. We also review the numerous antiviral prophylactic or pre-emptive treatments in use to control CMV infection, and suggest that they do not limit immune reactions leading to graft rejection or lower the risk of developing post-transplantation atherosclerosis in allograft recipients. Finally, we emphasise the need for prospective, international studies to clarify the role of infections in transplant rejection, to look at virus-to-virus interactions, and to establish specific therapeutic strategies. Such strategies must not rely exclusively on expensive antiviral agents but also on vaccination or other, innovative approaches, such as the use of agents able to inhibit the activity of natural killer cells, which might have an important role in acute allograft rejection.
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PMID:Infections and solid organ transplant rejection: a cause-and-effect relationship? 2355 27

Controlled trials suggest that acyclovir/valacyclovir can provide significant clinical benefits when used for prophylaxis in the immunocompromised host. These findings implicate herpesvirus(es) in the pathogenesis of complex medical conditions, including graft rejection and death. However, it is not known which of the 8 herpesviruses are important under particular circumstances. Prime candidates for triggering adverse outcomes are cytomegalovirus (CMV) in solid organ transplant recipients (causing rejection), CMV and human herpesvirus type 6 (HHV-6) in bone marrow transplant patients (causing marrow suppression), and herpes simplex virus, HHV-6, and CMV in AIDS patients (accelerating the rate of human immunodeficiency virus disease progression and death). Other diseases that may have a herpesvirus component or trigger susceptible antiviral agents include atherosclerosis and multiple sclerosis. In the future, clinicians should be alert to novel findings of randomized trials that may provide insight into the pathogenesis of these diseases and the contributions made by clinically silent herpesvirus infections.
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PMID:Tomorrow's challenges for herpesvirus management: potential applications of valacyclovir. 1235 98

Our previous study on herpesvirus infection including Herpes simplex virus type 1 (HSV-1), Epstein-Barr virus (EBV), cytomegalovirus (CMV) and atherosclerosis revealed that the prevalence of herpesvirus is higher in atherosclerotic aorta than in non-atherosclerotic aorta. Infections with two or three forms of the virus have been found only in atherosclerotic aorta. In our current study, we examined both Chlamydia pneumoniae and Chlamydia trachomatis in herpesvirus-infected aortic tissues, by means of immunohistochemistry, polymerase chain reaction, Southern hybridization, in situ hybridization, electron microscopy and electron-microscopic immunohistochemistry. In particular, the bacteria were found in atherosclerotic lesions. In atherosclerotic aorta, 40% of tissues examined were positive for C. pneumoniae in contrast to absence of this bacteria in non-atherosclerotic aorta. Elementary bodies of C. pneumoniae were found in macrophage-like cells in the intima of atherosclerotic aorta by electron microscopy. Chlamydia trachomatis was not found in both atherosclerotic and non-atherosclerotic aorta. Our findings suggest that multiple infections in aortic tissue contribute to the development of atherosclerosis. Furthermore, the absence of C. pneumoniae compared to herpesviruses in normal arterial tissue suggests that C. pneumoniae is specific for atherosclerotic lesions. In contrast to 'abortive infection' of viruses in arteries, C. pneumoniae infection was demonstrated in macrophages by electron microscopy and electron-microscopic immunohistochemistry in atherosclerotic lesion. Chlamydia pneumoniae may be the most important pathogen related to the development of atherosclerosis.
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PMID:Chlamydia pneumoniae and multiple infections in the aorta contribute to atherosclerosis. 1451 27

Atherosclerosis is a major health problem in industrialised countries. Several studies have suggested an association exists between certain microorganisms and the development of atherosclerosis. The aim of the study presented here was to assess the presence of viral or bacterial DNA in carotid atherosclerotic lesions. Nucleic acids were extracted from 18 carotid atherosclerotic lesions that had been collected surgically. Polymerase chain reaction was used to screen for specific genomic DNA from Chlamydia pneumoniae, cytomegalovirus and herpes simplex virus types 1 and 2. An original approach, based on the amplification by PCR of conserved bacterial 16S rDNA nucleotide sequences was also used to detect any bacterial species. The amplification product was identified by sequencing. Chlamydia pneumoniae, cytomegalovirus and herpes simplex 2 DNA were not detected in any of the samples. Herpes simplex 1 DNA was detected in 3 of the 18 samples. Genes encoding bacterial 16S rRNA were amplified and sequenced in eight atherosclerotic lesions. DNA sequences were identified by comparison with sequences registered in the GenBank database. These eight carotid atherosclerotic lesions were shown to contain several bacterial species belonging to human flora or the environment. The exact role of these microorganisms in the genesis or development of the atherosclerotic lesions remains unclear, but they may increase the inflammatory process or be an epiphenomenon.
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PMID:Viral and bacterial DNA in carotid atherosclerotic lesions. 1262 83

Viral infection of the vascular wall cellular elements is involved in development of several pathophysiological events, including vasculitis, transplant rejection, and atherosclerosis. Previously, we have shown that cultured human vascular endothelial cells (ECs) may be effectively infected with herpes simplex type I virus (HSV-1), and this cultural model could be a useful tool for the explanation of many aspects of viral disease. In this study, we investigated the effects of conditioned media (CM) of peripheral blood mononuclear cells (PBMCs) on HSV-1 reproduction and cell adhesion molecule expression in cultured ECs. PBMC-CM induced the delay of virus reproduction or inhibition of virus reproduction. Effects of CM correlated with multiplicity of infection used for EC, time of PBMC contact with infected and glutaraldehyde-fixed endothelium, and the level of IFNs and cytokine production. Passages of and CM-treated and infected cells without signs of virus reproduction were, sometimes, followed by virus reactivation. However, at a low level of infection of CM-treated ECs the virus reactivation was not observed even after 2-3 cell passages. Neutralizing antibodies against IFN-alpha, IFN-gamma, and TNF-alpha, used separately or together, significantly abrogated the delaying and/or inhibiting action of CM. Additionally, PBMC-CM significantly increased the expression of ICAM-1 and VCAM-1 on cultured ECs. The strongest cell activation was induced by CM obtained from PBMCs co-incubated with virus-infected endothelium. Obtained results suggest that primed leukocytes produce soluble factors with either anti-viral or pro-inflammatory activity, and the effect of PBMC-CM may have a bi-directional action. On the one hand, due to production of interferons and several cytokines CM sets up HSV-1 latency or virus elimination from cultured cells. On the other, the same cytokines act on infected and/or neighboring ECs and initiate the cascade of inflammatory reactions in the vascular wall.
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PMID:Herpes simplex type I virus infected human vascular endothelial cells induce the production of anti-viral and proinflammatory factors by peripheral blood leukocytes in vitro. 1268 53

Oxidative stress has been associated with a variety of pathologic conditions in humans. Increasing the transcriptional activities of antioxidant enzymes might be a strategy to prevent oxidative stress-associated diseases such as atherosclerosis and cancer. In the present paper, we studied the effects of extracts from 12 Mauritian endemic plants on the promoter activities of antioxidant enzymes; Cu, Zn-superoxide dismutase (Cu,Zn-SOD), Mn-superoxide dismutase (Mn-SOD), catalase, and glutathione dismutase (GPx). The levels of total phenolic compounds, total flavonoids, and proanthocyanidins were measured. Four luciferase expression vectors (pGL3-Basic) with promoter region of each enzyme were constructed, transfected to COS7 cells followed by an exposure to each extract (25 microg/ml, 24h, non-toxic dose). Thereafter, luciferase activities were evaluated in comparison with a control luciferase vector with a herpes simplex virus thymidine kinase promoter. Mauritian endemic plants contained high amounts of total phenols, flavonoids and proanthocyanidins. Total phenols and flavonoids were proportionally associated with Cu,Zn-SOD promoter activity, whereas they were inversely correlated with catalase promoter activity. These results suggest that the chemopreventive potentials of the extracts might reside in their abilities to modulate the expression of the antioxidant enzyme genes.
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PMID:Effects of the phenolic contents of Mauritian endemic plant extracts on promoter activities of antioxidant enzymes. 1470 34

Three infectious agents have recently gained considerable interest as potential pathogens in atherosclerosis and in its clinical manifestations: herpes simplex virus, cytomegalovirus, and Chlamydia pneumoniae. Chronic and often asymptomatic infections with these agents occur widely in the general population. These pathogens may affect atherosclerosis either directly or indirectly. Direct effects on vascular wall cells might include cell lysis, transformation, lipid accumulation, proinflammatory changes, and augmentation of procoagulant activity. Indirect systemic effects may involve induction of acute-phase proteins, establishment of a prothrombotic state, hemodynamic stress caused by tachycardia, increased cardiac output, or a regional inflammatory activation in response to systemic endotoxemia and cytokinemia. The effects of microbial infection, usually in combination with other risk factors (for example, smoking, hyperlipidemia, family history), might promote atherogenesis and eventually trigger acute coronary events.
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PMID:The mechanisms by which infectious agents may contribute to atherosclerosis and its clinical manifestations. 1498 64

The relative significance of traditional risk factors, chronic infections and autoimmune processes in the development of acute myocardial infarction (AMI) has not been fully elucidated. We compared serum IgG antibody titres to various pathogens, i.e. Chlamydia pneumoniae (Cpn), cytomegalovirus (CMV) and herpes simplex virus type 1 (HSV-1), and to the potential autoantigens human heat shock protein 60 (hHSP60) and mycobacterial heat shock protein 65 (mHSP65), in serum samples obtained from patients 3-48 h after AMI (n = 40) or stable effort angina (SEA, n = 43), and from controls (n = 46). The strongest association was observed between AMI and the elevated level of hHSP60 antibodies. The association between AMI and the level of Cpn antibodies was also significant. High levels of hHSP60 and Cpn antibodies represented independent risk factors for the development of AMI, but the simultaneous presence of high levels of antibodies to Cpn and hHSP60 suggested a joint effect on the relative risk of AMI (OR = 12.0-21.1). The antibody titres to mHSP65 were higher in the SEA group than in the controls, and the simultaneous presence of high levels of Cpn and mHSP65 antibodies meant an increased risk among the SEA patients. The antibody titres to CMV or HSV-1 were similar in the three groups. In conclusion, these results demonstrate associations of AMI with high levels of anti-hHSP60 and anti-Cpn antibodies, and of SEA with the level of anti-mHSP65 antibodies, these being independent risk factors.
Atherosclerosis 2004 Apr
PMID:Elevated antibody levels against Chlamydia pneumoniae, human HSP60 and mycobacterial HSP65 are independent risk factors in myocardial infarction and ischaemic heart disease. 1506 11

chlamdAs with other organ systems, the vulnerability of the nervous system to infectious agents increases with aging. Several different infectious agents can cause neurodegenerative conditions, with prominent examples being human immunodeficiency virus (HIV-1) dementia and prion disorders. Such infections of the central nervous system (CNS) typically have a relatively long incubation period and a chronic progressive course, and are therefore increasing in frequency as more people live longer. Infectious agents may enter the central nervous system in infected migratory macrophages, by transcytosis across blood-brain barrier cells or by intraneuronal transfer from peripheral nerves. Synapses and lipid rafts are important sites at which infectious agents may enter neurons and/or exert their cytotoxic effects. Recent findings suggest the possibility that infectious agents may increase the risk of common age-related neurodegenerative disorders such as Alzheimer's disease (AD) and Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and stroke. While scenarios can be envisioned whereby viruses such as Chlamydia pneumoniae, herpes simplex and influenza promote damage to neurons during aging, there is no conclusive evidence for a major role of these pathogens in neurodegenerative disorders. In the case of stroke, blood vessels may be adversely affected by bacteria or viruses resulting in atherosclerosis.
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PMID:Infectious agents and age-related neurodegenerative disorders. 1516 5


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