Linked Life Data

9780254

Source:http://linkedlifedata.com/resource/pubmed/id/9780254

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1998-12-10
pubmed:abstractText
Virus-enhancing factors present in the female genital tract may influence the transmission of human immunodeficiency virus type 1 (HIV-1). Previously, the presence of a heat-stable soluble factor in the cervicovaginal lavage (CVL) fluid of both HIV-infected and -uninfected women that induces HIV-1 expression in T cells and monocytes was reported. Now this CVL factor was shown to increase HIV-1 gene expression through the activation of the kappaB enhancer in the viral long terminal repeat (LTR). DNA binding studies, together with functional studies using mutant LTR reporter constructs, indicate the requirement for an NF-kappaB-dependent pathway in the CVL-mediated activation of HIV-1 expression. CVL samples that activated HIV-1 expression also stimulated AP-1-dependent transcription. These data demonstrate that an HIV-inducing factor, distinct from heat-labile cytokines, present in the female genital mucosa can activate AP-1 and NF-kappaB and increase HIV-1 gene expression through the kappaB enhancer, possibly contributing to HIV-1 transmission.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-1899
pubmed:author
pubmed:issnType
Print
pubmed:volume
178
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1343-51
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
A human immunodeficiency virus (HIV)-inducing factor from the female genital tract activates HIV-1 gene expression through the kappaB enhancer.
pubmed:affiliation
Department of Immunology, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois, USA. lalharth@rush.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't