Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2008-5-6
pubmed:abstractText
Infection of resting peripheral mononuclear blood cells (PBMCs) with HIV-1 is not productive due to a block prior to integration of the provirus into the host genome. Here we show that a unique restriction is determined by the status of the glucocorticoid receptor (GR). Proviral integration increases after addition of a GR ligand. The ligand dependent effect is confined to an early time period after infection and requires GR and the GR binding viral protein Vpr. Endogenous GR and transiently expressed Vpr are localized in the cytoplasm in unstimulated PMCs and comigrate into the nucleus upon ligand addition. Thus, the predominant cytoplasmic localization of GR seems to be a specific obstacle for HIV replication. Accordingly, efficient proviral integration in a cell line with a constitutive cytoplasmic GR requires addition of a GR ligand. The data suggest that steroids can overcome the restriction on HIV provirus formation and thereby increase the reservoir of virus producing cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0042-6822
pubmed:author
pubmed:issnType
Print
pubmed:day
25
pubmed:volume
375
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
73-84
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Activation of the glucocorticoid receptor releases unstimulated PBMCs from an early block in HIV-1 replication.
pubmed:affiliation
Heinrich-Pette-Institut für Experimentelle Virologie und Immunologie an der Universität Hamburg, 20251 Hamburg, Germany. wiegers@hpi.uni-hamburg.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't