@article{Estaquier2002Effec-14291,
  year={2002},
  doi={10.1128/JVI.76.12.5966-5973.2002},
  title={Effects of antiretroviral drugs on human immunodeficiency virus type 1-induced CD4(+) T-cell death},
  number={12},
  volume={76},
  issn={0022-538X},
  journal={Journal of Virology},
  pages={5966--5973},
  author={Estaquier, Jérôme and Lelièvre, Jean-Daniel and Petit, Frédéric and Brunner, Thomas and Moutouh-de Parseval, Laure and Richman, Douglas D. and Ameisen, Jean Claude and Corbeil, Jacques}
}

<rdf:RDF
    xmlns:dcterms="http://purl.org/dc/terms/"
    xmlns:dc="http://purl.org/dc/elements/1.1/"
    xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"
    xmlns:bibo="http://purl.org/ontology/bibo/"
    xmlns:dspace="http://digital-repositories.org/ontologies/dspace/0.1.0#"
    xmlns:foaf="http://xmlns.com/foaf/0.1/"
    xmlns:void="http://rdfs.org/ns/void#"
    xmlns:xsd="http://www.w3.org/2001/XMLSchema#" > 
  <rdf:Description rdf:about="https://kops.uni-konstanz.de/server/rdf/resource/123456789/14291">
    <dc:contributor>Brunner, Thomas</dc:contributor>
    <dc:creator>Lelièvre, Jean-Daniel</dc:creator>
    <dcterms:title>Effects of antiretroviral drugs on human immunodeficiency virus type 1-induced CD4(+) T-cell death</dcterms:title>
    <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dc:creator>Richman, Douglas D.</dc:creator>
    <dc:rights>terms-of-use</dc:rights>
    <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-10-21T08:19:02Z</dc:date>
    <foaf:homepage rdf:resource="http://localhost:8080/"/>
    <dc:creator>Ameisen, Jean Claude</dc:creator>
    <bibo:uri rdf:resource="http://kops.uni-konstanz.de/handle/123456789/14291"/>
    <dc:contributor>Lelièvre, Jean-Daniel</dc:contributor>
    <dc:creator>Moutouh-de Parseval, Laure</dc:creator>
    <dc:creator>Petit, Frédéric</dc:creator>
    <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dc:contributor>Richman, Douglas D.</dc:contributor>
    <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/>
    <dc:creator>Estaquier, Jérôme</dc:creator>
    <dcterms:hasPart rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/14291/2/2002_Estaquier_5966_Effects%20Antiretroviral.pdf"/>
    <dc:creator>Brunner, Thomas</dc:creator>
    <dc:contributor>Petit, Frédéric</dc:contributor>
    <dc:creator>Corbeil, Jacques</dc:creator>
    <dc:contributor>Corbeil, Jacques</dc:contributor>
    <dc:contributor>Moutouh-de Parseval, Laure</dc:contributor>
    <dcterms:bibliographicCitation>First publ. in: Journal of Virology ; 76 (2002), 12. - S. 5966-5973</dcterms:bibliographicCitation>
    <dc:language>eng</dc:language>
    <dcterms:issued>2002</dcterms:issued>
    <dcterms:abstract xml:lang="eng">Apoptosis of peripheral blood T cells plays an important role in the pathogenesis of human immunodeficiency virus (HIV) infection. In this study, we found that HIV type 1 (HIV-1) primes CD4+ T cells from healthy donors for apoptosis, which occurs after CD95 ligation or CD3-T-cell receptor (TCR) stimulation. CD95-mediated death did not depend on CD4 T-cell infection, since it occurred in the presence of the reverse transcriptase inhibitor didanosine (ddI). In contrast, apoptosis induced by productive infection (CD3-TCR stimulation) is prevented by both CD95 decoy receptor and ddI. Our data suggest that HIV-1 triggers at least two distinct death pathways: a CD95-dependent pathway that does not require viral replication and a viral replication-mediated cell death independent of the CD95 pathway. Further experiments indicated that saquinavir, a protease inhibitor, at a 0.2 µM concentration, decreased HIV-mediated CD95 expression and thus cell death, which is independent of its role in inhibiting viral replication. However, treatment of peripheral blood mononuclear cells from healthy donors with a higher concentration (10 µM) of an HIV protease inhibitor, saquinavir or indinavir, induced both a loss in mitochondrial membrane potential ({Delta}{Psi}m) and cell death. Thus, protease inhibitors have the potential for both beneficial and detrimental effects on CD4+ T cells independent of their antiretroviral effects.</dcterms:abstract>
    <dspace:hasBitstream rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/14291/2/2002_Estaquier_5966_Effects%20Antiretroviral.pdf"/>
    <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-10-21T08:19:02Z</dcterms:available>
    <dc:contributor>Estaquier, Jérôme</dc:contributor>
    <dcterms:rights rdf:resource="https://rightsstatements.org/page/InC/1.0/"/>
    <dc:contributor>Ameisen, Jean Claude</dc:contributor>
  </rdf:Description>
</rdf:RDF>