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)

Of four groups of chickens, two (groups I and II) were infected with MDV and two were not (groups III and IV). Groups I and III were fed diets low in lipid, and groups II and IV were fed cholesterol-supplemented diets. Striking grossly visible atherosclerotic lesions were seen in large coronary arteries, aortas, and major aortic branches of infected normocholesterolemic and hypercholesterolemic chickens (groups I and II). In contrast, grossly visible atherosclerotic lesions were not seen in uninfected normocholesterolemic chickens (group III), nor in uninfected hypercholesterolemic chickens (group IV). Microscopically, arterial changes in the infected animals were characterized by occlusive fibromuscular intimal thickening which formed fibrous caps overlying areas of atheromatous change. This change closely resembled chronic atherosclerosis in man. These results may have important bearing on our understanding of the etiology and pathogenesis of human arteriosclerosis since there is widespread and persistent infection of human populations with up to five different herpes-viruses.
 ...
PMID:Virus-induced atherosclerosis. 20 24

Several pieces of evidence suggest that vascular endothelium may be a site of latent herpetic viral infection, and that activation of such infection might cause or aggravate atherosclerosis. The present studies which utilized HSV-1 infection of cultured endothelial monolayers, provide insights into two phenomena seemingly relevant in considerations of atherosclerosis. Thus, mechanisms are reported by which infected endothelium may be damaged by marginated inflammatory cells, and be transformed from an anticoagulant to a procoagulant tissue. First, granulocytes are attracted to, and avidly bind, endothelium infected for very brief periods. This interaction is associated with denudation of intact cells as well as actual cytolysis through release of PMN proteases and toxic oxygen species. Second, several potentially additive abnormalities of HSV-infected endothelium would seem to foster coagulation. These include: a) its loss of surface heparans and thrombomodulin; b) its inability to synthesize prostacyclin with associated incapacity to deter platelet adhesion; c) its disordered membrane lipid conformation which is likely associated with excessive surface thrombin generation; and d) its unique ability to generate and release tissue factor. We speculate that mechanical abrasion may reactivate latent herpes (HSV or CMV) infection in endothelial cells particularly those exposed to high shear forces--for instance, at vessel bifurcations. This may underlie the endothelial damage, clotting and atheroma formation commonly found at these sites.
 ...
PMID:Herpes virus infection of endothelium: new insights into atherosclerosis. 132 3

It has been reported that atherosclerotic lesions contain genomic material belonging to members of the herpes family. This suggests that latent viral infection may be one of the atherogenic triggers. In this study we show that early infection of endothelial cell monolayers with Herpes Simplex virus type 1 (HSV-1) or Cytomegalovirus (CMV) results in an increased monocyte (MC) and polymorphonuclear leukocyte (PMN) adherence, but not in an increased platelet adhesion. Further, is demonstrated that MC and PMN respond differently to virus infected endothelial cell monolayers: PMN adhesion to CMV infected cells is approximately 430% of the control adherence, while the MC adherence is increased to 160%. Also, a difference in virus acting is observed: the adherence of MC or PMN to HSV-1 infected endothelial cells is caused by a secreted adherence promoting factor, while the adherence of MC or PMN to CMV infected endothelial cells seems to be a cell-bound phenomenon. In addition, it was demonstrated that the augmentation of MC or PMN adherence to virus infected endothelial cells is sensitive to tunicamycin, suggesting that both virus infections induce the expression of glycoproteins on the endothelial cell membrane, which is responsible for the MC and PMN adhesion. Thus, HSV-1 and CMV infection of endothelium results in an increased adherence of leukocytes which is suggested, irrespective of the precise nature of the mechanism of virus induced atherosclerosis, to be the earliest event associated with endothelium cell damage.
 ...
PMID:The effect of virus infection on the adherence of leukocytes or platelets to endothelial cells. 165 7

Clinical, epidemiological and serological data as well as literature reviews were used to formulate and substantiate a concept on the presence of cause-sequel (etiological) relation between chronic persistent (slow) infection caused by the Epstein-Barr herpes virus (chronic infectious mononucleosis) and atherosclerosis. Detailed findings of the etiologic agent of atherosclerosis makes it possible to plan principally new ways of its diagnosis, treatment and prophylaxis.
 ...
PMID:[Atherosclerosis and chronic persistent virus infection]. 196 33

Latent infection of vascular cells with herpes-viruses may play a pathogenic role in the development of human atherosclerosis. In a previous study, we found that cultured human umbilical vein endothelial cells (HUVECs) infected with herpes simplex virus 1 (HSV-1) became procoagulant, exemplified both by their enhanced assembly of the prothrombinase complex and by their inability to reduce adhesion of platelets. We now report two further procoagulant consequences of endothelial HSV infection: loss of surface thrombomodulin (TM) activity and induction of synthesis of tissue factor. Within 4 hr of infection of HUVECs, TM activity measured by thrombin-dependent protein C activation declined 21 +/- 3% (P less than 0.05) and by 18 hr, 48 +/- 5% (P less than 0.001). Similar significant TM decrements accompanied infection of bovine aortic endothelial cells. Identical TM loss was induced with HSV-2 infection but not with adenovirus infection. Decreased surface expression of TM antigen (measured by the specific binding of a polyclonal antibody to bovine TM) closely paralleled the loss of TM activity. As examined by Northern blotting, these losses apparently reflected rapid onset (within 4 hr of HSV infection) loss of mRNA for TM. In contrast, HSV infection induced a viral-dose-dependent increase in synthesis of tissue factor protein, adding to the procoagulant state. The results indicate that loss of endothelial protein-synthetic capacity is not a universal effect of HSV infection. We suggest that the procoagulant state induced by reduction in TM activity and amplified tissue factor activity accompanying HSV infection of endothelium could contribute to deposition of thrombi on atherosclerotic plaques and to the "coagulant-necrosis" state that characterizes HSV-infected mucocutaneous lesions.
 ...
PMID:Infection of vascular endothelial cells with herpes simplex virus enhances tissue factor activity and reduces thrombomodulin expression. 216 19

Experimental studies in chickens have shown a relationship of a herpesvirus to atherosclerosis. The hypothesis of an association in humans was tested by using data on the history of cold sores and other manifestations of herpes infections reported by 658 male and 919 female participants (ages 58 to 89) in the Framingham Heart Study from 1977 to 1979 and on the prevalence and subsequent 6-year incidence of coronary heart disease (CHD). Approximately 40% of the men and 52% of the women reported a history of ever having "fever blisters or cold sores." Overall, there was no association between a history of such oropharyngeal manifestations and prevalent CHD. Only in the subgroup of women with recurrent infections was there a suggestion of a possible relationship (relative risk = 1.5, 95% confidence interval 1.0 to 2.1). Among members of the cohort without CHD at baseline there was no association between the history of cold sores, chicken pox, shingles, or infectious mononucleosis and 6-year CHD incidence. However, a possible interaction among women with recurrent herpes, lower levels of serum cholesterol, and incidence of angina pectoris without myocardial infarction was suggested in post hoc analyses. These data from the Framingham cohort do not support the notion that any self-reported clinically manifest herpesvirus infection has a strong etiological role in older persons, but they do raise issues to be addressed in any further research.
 ...
PMID:Unlikely association between clinically apparent herpesvirus infection and coronary incidence at older ages. The Framingham Heart Study. 255 99

Genetically selected lines of Japanese quail, highly susceptible (SUS) and resistant (RES) to atherosclerosis, were used to study the possible involvement of Marek's disease herpes virus (MDV). An EcoRI gene library of MDV cloned in pBR328 was used to prepare the 32P-DNA probe in dot-blot and Southern blot hybridizations to detect the presence of MDV DNA sequence in the aorta, embryo and other tissue specimens. The viral DNA was found present in the aorta of SUS quail and it increased with the severity of the aortic lesion. For the DNA isolated from the atherosclerotic aorta, the endonuclease restriction map is specific but not identical to MDV genome. When screening the embryos of SUS and RES quail, it was found that all the SUS were positive with approximately 10 or more viral genome equivalents or virus copies per cell. The RES embryos were heterogeneous, 41% negative (less than 0.1 copy per cell), 43% intermediate (1-10 copies per cell) and 16% positive (10 or more copies per cell). The vaccination of SUS quail with the herpes virus of turkey vaccine did not prevent the disease. These results indicated that a part of MDV genome or another related herpes virus genome was integrated into the host DNA of SUS quail. The integrated viral gene or genes are believed to be important in atherogenesis, because they are genetically co-selected with the atherosclerosis-susceptibility.
Atherosclerosis 1987 Nov
PMID:Detection of specific DNA segments of Marek's disease herpes virus in Japanese quail susceptible to atherosclerosis. 282 27

The presence of herpes simplex virus (HSV) and cytomegalovirus (CMV) nucleic acid and/or antigen was demonstrated in the coronary arteries and thoracic aortas of young trauma victims by the in situ DNA hybridization and ABC immunoperoxidase methods, respectively. Epstein-Barr virus (EBV) nucleic acid and capsid antigen were not detected in the arteries sampled in this study. Of 8 subjects in which virus was detected in the coronary arteries, 6 were positive for HSV and 2 for CMV; of 7 cases positive in the thoracic aorta, 5 were identified as HSV and 2 as CMV. Viral DNA and/or antigen were found in occasional cells in the intact luminal surface and in focal clusters of spindle-shaped or "foamy" cells in the intimal layer. The histologic findings indicate that HSV and CMV are associated with areas showing early or advanced atheromatous changes in the coronary arteries and with lesion-free as well as lesion areas in the thoracic aorta. The virologic findings support the concept that herpes-viruses may potentially play a direct or indirect role in the pathogenesis of human atherosclerosis.
 ...
PMID:Herpesviridae in the coronary arteries and aorta of young trauma victims. 282 95

Infection with a human herpes virus, particularly cytomegalovirus (CMV), has been hypothesized to be a cofactor in the development of atherosclerosis in humans. We investigated the association of prior CMV infection with the presence of atherosclerosis in the coronary arteries of the native heart of 314 individuals undergoing heart transplantation. Age, male gender, race, tobacco use, and previous general and cardiac surgery were also studied as covariables. Factors associated with the presence of coronary atherosclerosis by univariate analysis were age greater than the median of 48 years (odds ratio [OR] = 5.9, 95% confidence intervals [CI] 3.0-11.6; P < 0.0001), tobacco use (OR = 3.8, 95% CI 2.1-7.0; P < 0.005), CMV seropositivity (OR = 3.1, 95% CI 1.8-5.5; P < 0.001), and male gender (OR = 3.0, 95% CI 1.6-5.4; P < 0.0005). When patients were divided into quartiles based on age, coronary atherosclerosis was shown to be associated with CMV seropositive status only in the youngest quartile of patients (OR = 3.6, 95% CI 1.4-8.9; P < 0.01) but not in the older three quartiles of patients (OR = 0.9, 95% CI = 0.3-2.4; P > 0.5). In multiple logistic regression analyses, CMV seropositivity was not a significant independent variable in the whole group of patients (P = 0.13) but remained a significant variable in the youngest quartile of patients (P = 0.01). However, 43% of these younger patients and 29% of all patients with coronary atherosclerosis were seronegative for CMV.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Investigation of cytomegalovirus infection as a risk factor for coronary atherosclerosis in the explanted hearts of patients undergoing heart transplantation. 785 75

Herpes ophthalmicus (HO) patients were examined for lipid spectrum of the serum. The tests revealed dyslipidemia (DLE) with a distinctive rise in the levels of total cholesterol (CS), alpha-CS and beta-CS. The severity of the lipidemic shifts correlated with that of the infection. DLE was more marked in recurrent HO. Clinical evidence was consistent with experimental findings. In rabbit models, herpetic keratoconjunctivitis was characterized by pronounced lipidemic alterations correctable with antiherpetic drug furavir. The results are discussed in terms of herpetic infection pathogenesis and its role in the development of atherosclerosis.
 ...
PMID:[Dyslipidemia in herpetic infection]. 790 19


1 2 3 4 5 Next >>