Linked Life Data

1320406

Source:http://linkedlifedata.com/resource/pubmed/id/1320406

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3 Pt 2
pubmed:dateCreated
1992-8-13
pubmed:abstractText
In conclusion, a great deal of indirect and inferential data point to herpesviruses as having a role in atherogenesis. It has been shown that the herpesviruses are able to remain within vascular tissue in a latent state, allowing for reactivation to occur with subsequent sequelae of an active infection. Herpesviruses affect the cellular metabolic activity of cells, induce the accumulation of lipids, and inhibit the production of matrix proteins. They have the ability to inhibit endothelial cell binding to the basement membrane. It is also known that the herpesviruses, particularly CMV, can initiate a variety of immunologic responses that may contribute to endothelial damage, precipitating atherogenesis. We are only beginning to understand how CMV may participate in ACAD. Greater attention must be focused on the exact cause-and-effect relationship between CMV infection and ACAD. Even the presence of CMV genomes in arterial walls of allografts must be viewed conservatively in the knowledge of CMV ubiquity and other probable contributions to ACAD. If CMV is involved in the development of ACAD, as an active or latent infection, directly or indirectly, it probably involves numerous coexistent mechanisms (Figure 5).
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
1053-2498
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
N
pubmed:pagination
S14-20
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:articleTitle
Cytomegalovirus and other herpesviruses: do they have a role in the development of accelerated coronary arterial disease in human heart allografts?
pubmed:affiliation
University of Nebraska Medical Center, Omaha 69198-6495.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't