Linked Life Data

7915148

Source:http://linkedlifedata.com/resource/pubmed/id/7915148

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1994-9-28
pubmed:abstractText
Cells of monocytic lineage (Mo) persistently infected with human immunodeficiency virus (HIV) have been suspected to be a major reservoir for in vivo transmission of virus to susceptible target cells. Cellular events and mechanisms that upregulate viral gene expression in such cells are important issues. Because the traffic of such cells is central to biodistribution of HIV, we have explored the impact of interaction of endothelium with HIV-1-infected U1 promonocytic cells. Coculturing of U1 with human umbilical endothelial cells (HUVEC) for 24 to 72 hours in the absence of stimulation induced HIV-1 p24 biosynthesis significantly. Antibody-blocking experiments indicated that CD11/CD18 integrins play a role in upregulation of HIV expression elicited by interaction with HUVEC. Engagement of CD11b/CD18 by adherence of U1 to surfaces coated with either the cognate ligand fibrinogen or monoclonal antibody specific for CD11b/CD18 also enhanced p24 biosynthesis. Furthermore, endothelial cells were found to constitutively synthesize and secrete soluble factors that enhanced HIV-1 synthesis. The enhancing factors, of estimated size 10 to 45 kD, were induced in HUVEC to high levels by monokines or by lipopolysaccharide, resulting in markedly enhanced HIV-1 expression by U1. These endothelial cell-derived HIV-1-enhancing factors consist of, among others, interleukin-6 (IL-6), IL-1 beta, and granulocyte-macrophage CSF (GM-CSF). Our results suggest that activation of HIV biosynthesis in infected Mo via interaction with endothelium may impact significantly on the tissue distribution and pathogenesis of HIV infections.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
84
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1567-72
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:7915148-Antibodies, Monoclonal, pubmed-meshheading:7915148-Antigens, CD, pubmed-meshheading:7915148-Antigens, CD11, pubmed-meshheading:7915148-Antigens, CD18, pubmed-meshheading:7915148-Cell Line, pubmed-meshheading:7915148-Cells, Cultured, pubmed-meshheading:7915148-Cytokines, pubmed-meshheading:7915148-Endothelium, Vascular, pubmed-meshheading:7915148-Granulocyte-Macrophage Colony-Stimulating Factor, pubmed-meshheading:7915148-HIV Core Protein p24, pubmed-meshheading:7915148-HIV-1, pubmed-meshheading:7915148-Humans, pubmed-meshheading:7915148-Interleukin-6, pubmed-meshheading:7915148-Kinetics, pubmed-meshheading:7915148-Lipopolysaccharides, pubmed-meshheading:7915148-Monocytes, pubmed-meshheading:7915148-Time Factors, pubmed-meshheading:7915148-Tumor Cells, Cultured, pubmed-meshheading:7915148-Tumor Necrosis Factor-alpha, pubmed-meshheading:7915148-Umbilical Veins, pubmed-meshheading:7915148-Virus Replication
pubmed:year
1994
pubmed:articleTitle
Upregulation of human immunodeficiency virus-1 in chronically infected monocytic cell line by both contact with endothelial cells and cytokines.
pubmed:affiliation
Department of Immunology, Scripps Research Institute, La Jolla, CA 92037.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S.