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

Herpesviruses have been implicated as etiologic factors in the pathogenesis of human arteriosclerosis. We have examined the pathobiological effects of human herpes simplex virus (HSV-1) infection in influencing lipid accumulation and metabolism in human and bovine arterial smooth muscle cells (SMC). Significantly greater amounts of saturated cholesteryl esters (CE) and triacylglycerols (TG) accumulate in HSV-1-infected human and bovine arterial SMC than uninfected cells. This CE accumulation results, in part, from decreased CE hydrolysis. Furthermore, arachidonate-stimulated, HSV-1-infected arterial SMC have a reduced capacity to produce prostacyclin (an agonist of intracellular CE hydrolytic activity) than uninfected, stimulated SMC. It appears that HSV-1 may induce lipid accumulation in arterial SMC similar, in part, to the lipid accumulation observed in vivo during human atherogenesis. Thus, herpesviruses may contribute to lipid accumulation, which is a characteristic feature of atherosclerosis.
 ...
PMID:Herpes simplex virus infection in human arterial cells. Implications in arteriosclerosis. 311 62

Arterial tissues from carotid artery plaques or from punch-biopsy samples of uninvolved areas of the aorta were removed from 132 patients with atherosclerosis during blood-vessel surgery. Cells morphologically identical to smooth muscle cells were cultured from 26 to 126 plaque samples and from 6 of 6 punch-biopsy samples. Immunofluorescence tests of these cells showed that more than 25% of the cell cultures from both types of sample contained antigens of human cytomegalovirus (CMV) but not of herpes simplex virus type 1 or type 2. Replicating CMV was not detected by electron microscopy in the antigen-positive cells, suggesting that the artery walls may be a site of CMV latency.
 ...
PMID:Cytomegalovirus antigen within human arterial smooth muscle cells. 613 95

Endothelial injury is important in the pathogenesis of thrombosis, atherosclerosis, disseminated intravascular coagulation, and vasculitis. The ability of several common human viruses to infect cultures of endothelial cells obtained from human umbilical veins or bovine thoracic aorta was demonstrated. Indicators of infection included cytopathology, viral growth curves, and antigen detection by immunofluorescence. Herpes simplex virus type 1, adenovirus type 7, measles virus, and parainfluenza virus type 3 infected both human venous and bovine aorta endothelium. Mumps virus, poliovirus type 1, and echovirus type 9 grew only in human venous cells; coxsackievirus B4 infected only bovine arterial cultures; and cytomegalovirus, influenza A/Victoria/75 (H3N2) virus, and respiratory syncytial virus failed to grow in either cell culture. During replication some viruses caused acute lytic changes; some produced chronic, less destructive alterations; and other induced no apparent cytopathology. The results suggest that viral replication within endothelium may be important in the pathogenesis of viral disease of initiation of vessel-wall injury.
 ...
PMID:Virus infection of endothelial cells. 626 Aug 74

To examine the possible role of viruses in the etiology of atherosclerosis, we searched for the presence of viral genomes in arterial tissues by in situ hybridization. Because chickens infected with Marek disease virus, a herpesvirus, develop atherosclerotic lesions after infection, we looked for the presence of herpesvirus or parts thereof in human artery wall tissue, particularly in individuals with evidence of atherosclerosis. Herpesvirus probes were used on specimens of aortic wall removed from patients undergoing coronary bypass surgery. Evidence for the presence of herpes simplex viral mRNA was obtained in 13 specimens. Some of the specimens positive for herpes simplex virus appear to represent early stages in atherogenesis. Evidence for the presence of cytomegalovirus or Epstein-Barr viral genome was not observed in any of the specimens examined. We have also shown that herpes simplex virus can infect human fetal smooth muscle cells in culture. There are several ways in which viruses could operate in the pathogenesis of atherosclerosis: They could induce proliferation of artery wall intimal smooth muscle cells via injury or by genomic alterations leading to clonal expansion of intimal smooth muscle cell populations. We suggest that expression of at least a part of the herpesvirus genome in arterial smooth muscle cells may in some cases be instrumental in initiating or maintaining this enhanced cell proliferation. Furthermore, viral agents could explain other puzzling features in the occurrence of atherosclerosis and the attendant heart disease and strokes.
 ...
PMID:Viruses in the etiology of atherosclerosis. 631 57

The authors found a significant reduction of the suppressor function in carriers of the Australian antigen. This may contribute to a formation of immune complexes. Infection of rabbits with Herpes simplex virus resulted in an essentially enhanced development of experimental atherosclerosis against the background of a reduction of the suppressor function. These findings give evidence of the importance of viral infection in the development of atherosclerosis due to an inhibition of the suppressor function of T lymphocytes.
 ...
PMID:[Influence of viral infections in the pathogenesis of atherosclerosis]. 813 Jan 63

This paper presents a brief overview of our current understanding of the relationship between herpes simplex virus (HSV) and atherogenesis. In the search for a viral trigger of atherosclerosis, several investigators reported the detection of herpes simplex virus in some, but not all atherosclerotic lesions. HSV infections are very common, not only in atherosclerotic patients but also in the general population, making epidemiological studies difficult to interpret. Different mechanisms by which HSV may contribute to atherogenesis have been described. In vascular cells, HSV infection leads to lipid accumulation. HSV infection of endothelial cells attracts leukocytes with subsequent inflammatory damage; it activates procoagulant changes on endothelium with increased thrombin generation and platelet adhesion, and changes its interaction with extracellular matrix proteins. Future studies should delineate whether these mechanisms are operative in the pathogenesis of atherosclerosis.
 ...
PMID:Herpes simplex virus and atherosclerosis. 813 86

Ubiquitous viruses such as members of the human herpes virus group, particularly cytomegalovirus (CMV), have been proposed to be clinically important agents in the initiation and progression of atherosclerosis. Antibodies to CMV and herpes simplex virus type 1 (HSV1) and type 2 (HSV2) were determined in 340 matched case-control pairs from the Atherosclerosis Risk in Communities (ARIC) Study. Cases were defined by B-mode ultrasonography as persons with thickened carotid artery walls consistent with early atherosclerosis but without a history of cardiovascular disease. Controls were defined as persons without thickened walls or history of cardiovascular disease. The case-control odds ratio for CMV antibodies was 1.55 (P = .03), for HSV 1.41 (P = .07), and for HSV2 0.91 (P = .63). When adjustment was made for potential confounders, the odds ratios were 1.36 for CMV (P = .24), 1.21 for HSV1 (P = .45), and 0.61 (P = .05) for HSV2. These results suggest a modest association between CMV and asymptomatic carotid wall thickening consistent with early atherosclerosis.
 ...
PMID:Cytomegalovirus/herpesvirus and carotid atherosclerosis: the ARIC Study. 830 17

Previous studies of age-related susceptibility to viral infection have focused largely on the effects of aging on the immune response. Little attention has been given to age-related changes in the infectivity of target cells. We show here a fourfold greater plating efficiency of herpes simplex virus type 1 (HSV-1) for cultured vascular smooth muscle cells derived from adult rats compared with cells from genetically identical pup rats. The difference in plating efficiency appeared to be due to differences in initial attachment of the virion to the cell surface. There were no differences in the rate of viral entry or the efficiency of viral replication at high multiplicities of infection and no resistant "subpopulation" of pup cells. The pup cells did not release a soluble inhibitor of infection. Infection in both cell types was inhibited similarly by basic fibroblast growth factor (bFGF). Although adult cells exhibited a more vigorous mitogenic response to bFGF than did pup cells, binding studies did not demonstrate significant differences in the binding of bFGF to the cell surface, suggesting that differential expression of high-affinity FGF receptors could not be correlated with the difference in infectivity. We speculate that differences in the distribution of heparan sulfate in the cell surface, which serves as the initial attachment site for HSV-1, may explain the observed differences in plating efficiency. Since age is a risk factor for the development of atherosclerosis, these results have potential implications for susceptibility of the vasculature to herpesviral infections as a function of the development of the vessel wall.
 ...
PMID:Developmentally regulated herpesvirus plaque formation in arterial smooth muscle cells. 838 74

A large body of evidence exists that implicates a number of microbial agents in the pathogenesis of coronary heart disease (CHD). This, if proven, may have far-reaching implications for the prevention and treatment of CHD and other atherosclerotic disease. The histopathology of atherosclerosis and its natural history suggest infectious causation at many points along the progression of disease, particularly with regard to CHD, and a number of pathogens have been the focus of study. Viral agents implicated include Coxsackie B4 virus, for which tenuous sero-epidemiological associations exist, and the Herpesviridae. The animal herpesvirus causing Marek's disease in chickens causes atherosclerotic lesions in these animals. Herpes simplex virus I and II have been found in aortic smooth muscle and produce changes in vitro in smooth muscle that are similar to those seen at the beginning of atherosclerosis and which may also explain some of the features of atherosclerotic complications. Cytomegalovirus is implicated more strongly sero-epidemiologically by in-vivo detection in atherosclerotic lesions and by its links with post-cardiac transplant vasculopathya syndrome similar to atherosclerosis. Bacteria have also been shown to have links with CHD. Chlamydia pneumoniae and Helicobacter pylori have both been associated sero-epidemiologically with CHD, and these findings have been consolidated by recent work showing their presence in atherosclerotic lesions in adults. Bacterial infections in general lead to many changes in lipid, thrombic and other acute-phase protein metabolism, and some of these changes occur with both C. pneumoniae and H. pylori infections. The ubiquity and similar epidemiological features to CHD of all these microbial pathogens make the resolution of the causative issue impossible by retrospective means. All that can be shown at present are a variety of weak and strong links, the significance of which can only be determined by large and perhaps lifetime prospective studies.
 ...
PMID:Infection and coronary heart disease. 923 36

Herpes simplex virus type 1 and cytomegalovirus alter the phenotype of the endothelium in vitro from anticoagulant to procoagulant, thereby promoting the adherence of neutrophils and platelets to the endothelium. Virus infection of the endothelium induces the expression of viral glycoproteins and adhesion molecules, which promote neutrophil and monocyte adhesion. Herpes simplex infection of the endothelium promotes prothrombinase assembly, allowing more efficient thrombin generation. Excess thrombin generation causes translocation of P-selectin. Viral infection also induces the procoagulant molecule, tissue factor, in endothelial cells. These enhanced procoagulant effects are associated with the loss of anticoagulants, including thrombomodulin, prostacyclin and tissue plasminogen activator. These studies support the speculation that virus infection in vivo promotes vascular injury and thrombosis, which may contribute to disease states such as atherosclerosis.
 ...
PMID:Effects of viral activation of the vessel wall on inflammation and thrombosis. 966 64


<< Previous 1 2 3 4 5 6 7 Next >>