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)

We examined 164 endomyocardial biopsy specimens from 29 patients who received an orthotopic heart transplant since 1984. Rejection was graded according to the Hannover classification. Non-isotopic in situ DNA hybridization was conducted on cryostat sections with biotinylated probes for herpes simplex virus, Epstein-Barr virus, and cytomegalovirus. Serial sections of 126 biopsies were investigated immunohistochemically for the presence of activated T lymphocytes and proliferating cells, with monoclonal antibodies against interleukin 2 receptors (CD 25) and Ki-67 antigen. Relations between rejection grades, presence of proliferating cells, and presence of herpesvirus DNA were determined for the total number of biopsies. For some patients correlation of these parameters was studied over time. Herpesviral nucleic acids were detected in 25% of all biopsies: 37% of biopsies with relevant rejection (grades A 2 or A 3; 39% of all biopsies) compared to 18% of biopsies graded A 0, A 1, or A 5 (61% of all samples) (P less than 0.01). 56% of the biopsies with infection showed relevant rejection as compared with only 33% of the uninfected. Ki-67 expression was found in 41% of all biopsies, mainly in infiltrating cells: 69% of biopsies with relevant rejection compared with 23% of cases of minor/no rejection (P much less than 0.001). Ki-67 expression was also associated with herpesvirus infection: 66% of infected biopsies contained Ki-67 positive cells compared with 33% of uninfected biopsies (P less than 0.001). Herpesvirus infection was usually observed within the interstitial cell population, which, in many cases, displayed a considerable Ki-67 expression, too. In few cases only, hybridization was unequivocally found in vascular wall cells or myocytes. Viral myocarditis does not only mimic graft rejection morphologically, but it may also affect the course of rejection, via induction of antigenic changes or direct injury of cardiac tissues. Virus infections may also elicit or aggravate obliterative coronary artery disease, and thus contribute to accelerated graft atherosclerosis.
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PMID:Rejection, herpesvirus infection, and Ki-67 expression in endomyocardial biopsy specimens from heart transplant recipients. 131 59

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.
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PMID:[Atherosclerosis and chronic persistent virus infection]. 196 33

The immune response against Cytomegalovirus (CMV) and Epstein-Barr virus (EBV)-induced antigens has been determined in teh sera of 36 patients with angiographically assessed atherosclerosis and compared with that of 36 matched control subjects. Significantly higher titres of antibody against CMV and EBV - induced antigens and a significant increase in CMV- and EBV- reactivated infections were found in atherosclerotic patients as compared to control subjects. Moreover serological signs of concomitant EBV and CMV infections occurred more frequently in atherosclerotic patients than in controls. One atherosclerotic patient, however, completely lacked antibody to CMV while CMV- and EBV- reactivated infections were also noted in control subjects, probably connected with their old age. Our data suggest that multiple reactivations of latent viruses may represent a consequence rather than a causal factor of atherosclerosis.
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PMID:Antibody patterns against cytomegalovirus and Epstein-Barr virus in human atherosclerosis. 215 75

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.
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PMID:Herpesviridae in the coronary arteries and aorta of young trauma victims. 282 95

We looked for antibodies against endothelial cells, monocytes, fibroblasts, lymphocytes and Epstein-Barr virus transformed lymphocytes in the sera of 28 elderly and 18 middle-aged patients with atherosclerotic peripheral arterial disease and 13 controls. Inclusion criteria were symptomatic peripheral arterial disease with intermittent claudication and ankle/radial Doppler pressure ratio less than 0.7 in the patient group and greater than 1 in the controls. The sera were tested using a standard cytotoxic technique against a cell panel of monocytes, T and B lymphocytes from 5 donors, and against endothelial cells, fibroblasts and Epstein-Barr virus transformed lymphocytes from one umbilical cord vein and blood. The sera of 30 of 46 (65.2%) patients showed toxicity against monocytes from at least one member of the cell panel and 12 of 19 sera tested (63%) reacted with endothelial cells. Only one of the control sera was positive against monocytes and none reacted with endothelial cells. None of the sera of either patients or controls contained cytotoxic antibodies against T and B lymphocytes, Epstein-Barr virus transformed lymphocytes or fibroblasts. The selective cytotoxicity suggests that the antibodies detected are not against HLA-antigens (which are expressed by normal lymphocytes and Epstein-Barr virus lymphocytes). Our results suggest that immune phenomena occur in atherosclerosis.
Atherosclerosis 1988 Nov
PMID:Antibodies against monocytes and endothelial cells in the sera of patients with atherosclerotic peripheral arterial disease. 326 60

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.
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PMID:Viruses in the etiology of atherosclerosis. 631 57

The Werner syndrome (WS) is a rare autosomal recessive progeroid syndrome characterized by the premature onset of multiple age-related disorders, including atherosclerosis, cancer, non-insulin-dependent diabetes mellitus (NIDDM), ocular cataracts and osteoporosis [Epstein et al., 1966]. The major cause of death (at a median age of 47) is myocardial infarction (MI) [Epstein et al., 1966]. The WS mutation involves a member (WRN) of the RecQ family of helicases and may perturb DNA replication, repair, recombination, transcription, or chromosomal segregation [Yu et al., 1996]. We now report data on 149 MI cases and age-matched controls suggesting that a polymorphic WRN variant is associated with increased risk for MI. Based on our data, homozygosity for a cysteine at amino acid 1367 (the most prevalent genotype) predicts a 2.78 times greater risk of MI (95% confidence intervals: 1.23 to 6.86). The variant was not significantly associated with NIDDM. The two alleles (cysteine vs. arginine) could influence helicase activity, turnover, macromolecular interactions or, alternatively, could be markers for haplotypes influencing WRN regulation or reflecting gene action at linked loci. However, given the caveats implicit in genetic association studies, it is imperative that the present results be replicated in independent populations.
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PMID:Association of a polymorphic variant of the Werner helicase gene with myocardial infarction in a Japanese population. 902 Oct 29

The objectives of the present study were to characterize the surface expression of low density lipoprotein receptor (LDL-R) in Epstein-Barr virus transformed lymphocytes (EBV-L) and to determine the applicability of the cellular system for the study of familial hypercholesterolemia. The EBV-L subsets and LDL-R expression were determined by immuno-cytofluorimetry. The LDL-R expression in EBV-L which consisted of mostly B cells was no different among antigenic subsets. EBV-L cultured in lipoprotein deficient serum demonstrated a 9.3-fold higher LDL-R expression than primary lymphocytes. Lovastatin caused an additional 1.9-and 1.4-fold increase in EBV-L and primary lymphocytes respectively. This difference in lovastatin response is statistically significant (paired t-test, P < 0.001). 54% of the high LDL-R expression in EBV-L was related to the changes in proliferation measured as stimulation index (SI). LDL and lovastatin modulated the LDL-R expression without affecting SI. FH subjects demonstrated 2% (homozygote, n = 1) and 44.6 +/- 12.3% (heterozygotes, n = 35) in LDL-R expression of controls (n = 30). This maintenance of the FH phenotype and the intrinsically high LDL-R expression in EBV-L make the cellular system suitable for the study of FH as well as the regulation of LDL-R.
Atherosclerosis 1997 Jun
PMID:Surface expression of low density lipoprotein receptor in EBV-transformed lymphocytes: characterization and use for studying familial hypercholesterolemia. 919 67

Malignant lymphoma infiltrating the abdominal aorta and resulting in an aortic aneurysm has never been documented. We report here a case of angiocentric T-cell lymphoma in a 33-year-old man who for months presented intermittent fever, splenomegaly, and an abdominal pulsatile mass. Angiography revealed extensive aneurysmal dilatation of the infrarenal abdominal aorta, bilateral iliac artery, and right common femoral artery. Splenic abscess and infected abdominal aortic aneurysm were initially suspected. An urgent splenectomy and aneurysmectomy with an aortic bifemoral bypass were performed. Pathological examination of the aortic aneurysm showed extensive necrosis, severe atherosclerosis, and lymphoma cell infiltration of the aortic wall. The lymphoid cells in the aorta and spleen were stained positive for CD45RO, CD56, and CD8, but negative for CD4 and CD19. Double-labeling immunohistochemistry and in situ hybridization using EBER1 for Epstein-Barr virus (EBV) revealed positive nuclear staining in the atypical T-lymphoid cells. This is the first definitive proof of peripheral T-cell lymphoma involving the abdominal aorta. Our evidence also supports that the EBV infection of T cells could be responsible for the atherosclerosis and hypertriglyceridemia, and the angiocentricity of the tumor cells apparently results in the presenting atherosclerotic aortic wall destruction, providing an additional causative concept for abdominal aortic aneurysm.
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PMID:Epstein-Barr virus-containing T-cell lymphoma and atherosclerotic abdominal aortic aneurysm in a young adult. 1049 49

Recent publications have suggested that infective pathogens might play an important role in the pathogenesis of atherosclerosis. This review focuses on these microorganisms in the process of atherosclerosis. The results of in vitro studies, animal studies, tissue studies, and serological studies will be summarised, followed by an overall conclusion concerning the strength of the association of the microorganism with the pathogenesis of atherosclerosis. The role of the bacteria Chlamydia pneumoniae and Helicobacter pylori, and the viruses human immunodeficiency virus, coxsackie B virus, cytomegalovirus, Epstein-Barr virus, herpes simplex virus, and measles virus will be discussed.
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PMID:Microorganisms in the aetiology of atherosclerosis. 1104 Oct 53


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