Linked Life Data

9918882

Source:http://linkedlifedata.com/resource/pubmed/id/9918882

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1999-2-17
pubmed:abstractText
To explore the possibility of conferring a long-term resistance against human immunodeficiency virus (HIV) by a low continuous production of interferon-beta (IFN-beta) in hematopoietic progenitor cells, we transduced the human CD34(+) TF-1 cells with a retroviral vector ensuring IFN-beta production. The IFN-beta-transduction of TF-1 cells resulted in resistance to infection with HIV-LAI, as shown by the selective survival of IFN-beta-transduced CD4(+) cells and the protection against HIV-induced apoptosis. A similar response against HIV-LAI infection was obtained after pretreatment with 100 U/ml of recombinant IFN-alpha2b or IFN-beta. In contrast, after the addition of macrophage cell tropic (M cell-tropic) HIV strain, a treatment with exogenous IFN-alpha2b resulted in a >==10-fold lower protection compared with exogenous IFN-beta or IFN-beta transduction. This specific effect of IFN-beta on M cell-tropic HIV strains was correlated with a down-regulation of the CCR-5 chemokine receptor expression, corresponding to a novel antiviral effect of IFN-beta.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0042-6822
pubmed:author
pubmed:copyrightInfo
Copyright 1999 Academic Press.
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
253
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
241-9
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Interferon-beta-induced human immunodeficiency virus resistance in CD34(+) human hematopoietic progenitor cells: correlation with a down-regulation of CCR-5 expression.
pubmed:affiliation
Centre National de la Recherche Scientifique, Institut Curie, Université Paris 11, Orsay, 91405, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't