Sequence evolution and escape from specific immune pressure of an HIV‐1 Rev epitope with extensive sequence similarity to human nucleolar protein 6
Identifieur interne : 002320 ( Main/Exploration ); précédent : 002319; suivant : 002321Sequence evolution and escape from specific immune pressure of an HIV‐1 Rev epitope with extensive sequence similarity to human nucleolar protein 6
Auteurs : S. D. Allard [Belgique] ; A. L. De Goede [Pays-Bas] ; B. De Keersmaecker [Belgique] ; C. Heirman [Belgique] ; P. Lacor [Belgique] ; A. D. M. E. Osterhaus [Pays-Bas] ; C. Demanet [Belgique] ; K. Thielemans [Belgique] ; R. A. Gruters [Pays-Bas] ; J. L. Aerts [Belgique]Source :
- Tissue Antigens [ 0001-2815 ] ; 2012-03.
Abstract
Antigen‐specific immunity is crucially important for containing viral replication in human immunodeficiency virus (HIV)‐1‐infected hosts. Several epitopes have been predicted for the early expressed HIV‐1 proteins Tat and Rev, but few have been studied in detail. We characterized the human leukocyte antigen (HLA)‐B44‐restricted Rev epitope EELLKTVRL (EL9) in an HIV‐1‐infected subject treated with antiretroviral therapy. Interestingly, a high sequence similarity was found between the EL9 epitope and the human nucleolar protein 6 (NOL6). However, this similarity does not seem to impede immunogenicity as CD8+ T‐cells, previously stimulated with EL9‐pulsed dendritic cells, were able to specifically recognize the HIV‐1 Rev epitope without cross‐recognizing the human self‐antigen NOL6. After the subject interrupted antiretroviral therapy and virus rebounded, mutations within the EL9 epitope were identified. Although the emerging mutations resulted in decreased or abolished T‐cell recognition, they did not impair Rev protein function. Mutations leading to escape from T‐cell recognition persisted for up to 124 weeks following treatment interruption. This study shows that the HLA‐B44‐restricted Rev CD8+ T‐cell epitope EL9 is immunogenic notwithstanding its close resemblance to a human peptide. The epitope mutates as a consequence of dynamic interaction between T‐cells and HIV‐1. Clinical status, CD4+ T‐cell count and viral load remained stable despite escape from T‐cell recognition.
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DOI: 10.1111/j.1399-0039.2012.01837.x
Affiliations:
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D." last="Allard">S. D. Allard</name><affiliation wicri:level="3"><country xml:lang="fr">Belgique</country><wicri:regionArea>Laboratory of Molecular and Cellular Therapy, Department of Physiology and Immunology, Medical School of the Vrije Universiteit Brussel, Brussels</wicri:regionArea><placeName><settlement type="city">Bruxelles</settlement><region nuts="2">Région de Bruxelles-Capitale</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">Belgique</country><wicri:regionArea>AIDS Unit, Department of Internal Medicine and Infectious Diseases, Universitair Ziekenhuis Brussel, Brussels</wicri:regionArea><placeName><settlement type="city">Bruxelles</settlement><region nuts="2">Région de Bruxelles-Capitale</region></placeName></affiliation></author><author><name sortKey="De Goede, A L" sort="De Goede, A L" uniqKey="De Goede A" first="A. L." last="De Goede">A. L. De Goede</name><affiliation wicri:level="3"><country xml:lang="fr" wicri:curation="lc">Pays-Bas</country><wicri:regionArea>Department of Virology, Erasmus Medical Center, Rotterdam</wicri:regionArea><placeName><settlement type="city">Rotterdam</settlement><region nuts="2" type="province">Hollande-Méridionale</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr" wicri:curation="lc">Pays-Bas</country><wicri:regionArea>Department of Hospital Pharmacy, Erasmus Medical Center, Rotterdam</wicri:regionArea><placeName><settlement type="city">Rotterdam</settlement><region nuts="2" type="province">Hollande-Méridionale</region></placeName></affiliation><affiliation wicri:level="1"><country wicri:rule="url">Pays-Bas</country></affiliation></author><author><name sortKey="De Keersmaecker, B" sort="De Keersmaecker, B" uniqKey="De Keersmaecker B" first="B." last="De Keersmaecker">B. 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Aerts</name><affiliation wicri:level="3"><country xml:lang="fr">Belgique</country><wicri:regionArea>Laboratory of Molecular and Cellular Therapy, Department of Physiology and Immunology, Medical School of the Vrije Universiteit Brussel, Brussels</wicri:regionArea><placeName><settlement type="city">Bruxelles</settlement><region nuts="2">Région de Bruxelles-Capitale</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Tissue Antigens</title><title level="j" type="alt">TISSUE ANTIGENS</title><idno type="ISSN">0001-2815</idno><idno type="eISSN">1399-0039</idno><imprint><biblScope unit="vol">79</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="174">174</biblScope><biblScope unit="page" to="185">185</biblScope><biblScope unit="page-count">12</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2012-03">2012-03</date></imprint><idno type="ISSN">0001-2815</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0001-2815</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Antigen‐specific immunity is crucially important for containing viral replication in human immunodeficiency virus (HIV)‐1‐infected hosts. Several epitopes have been predicted for the early expressed HIV‐1 proteins Tat and Rev, but few have been studied in detail. We characterized the human leukocyte antigen (HLA)‐B44‐restricted Rev epitope EELLKTVRL (EL9) in an HIV‐1‐infected subject treated with antiretroviral therapy. Interestingly, a high sequence similarity was found between the EL9 epitope and the human nucleolar protein 6 (NOL6). However, this similarity does not seem to impede immunogenicity as CD8+ T‐cells, previously stimulated with EL9‐pulsed dendritic cells, were able to specifically recognize the HIV‐1 Rev epitope without cross‐recognizing the human self‐antigen NOL6. After the subject interrupted antiretroviral therapy and virus rebounded, mutations within the EL9 epitope were identified. Although the emerging mutations resulted in decreased or abolished T‐cell recognition, they did not impair Rev protein function. Mutations leading to escape from T‐cell recognition persisted for up to 124 weeks following treatment interruption. This study shows that the HLA‐B44‐restricted Rev CD8+ T‐cell epitope EL9 is immunogenic notwithstanding its close resemblance to a human peptide. The epitope mutates as a consequence of dynamic interaction between T‐cells and HIV‐1. Clinical status, CD4+ T‐cell count and viral load remained stable despite escape from T‐cell recognition.</div></front></TEI><affiliations><list><country><li>Belgique</li><li>Pays-Bas</li></country><region><li>Hollande-Méridionale</li><li>Région de Bruxelles-Capitale</li></region><settlement><li>Bruxelles</li><li>Rotterdam</li></settlement></list><tree><country name="Belgique"><region name="Région de Bruxelles-Capitale"><name sortKey="Allard, S D" sort="Allard, S D" uniqKey="Allard S" first="S. D." last="Allard">S. D. Allard</name></region><name sortKey="Aerts, J L" sort="Aerts, J L" uniqKey="Aerts J" first="J. L." last="Aerts">J. L. Aerts</name><name sortKey="Allard, S D" sort="Allard, S D" uniqKey="Allard S" first="S. D." last="Allard">S. D. Allard</name><name sortKey="De Keersmaecker, B" sort="De Keersmaecker, B" uniqKey="De Keersmaecker B" first="B." last="De Keersmaecker">B. De Keersmaecker</name><name sortKey="Demanet, C" sort="Demanet, C" uniqKey="Demanet C" first="C." last="Demanet">C. Demanet</name><name sortKey="Heirman, C" sort="Heirman, C" uniqKey="Heirman C" first="C." last="Heirman">C. Heirman</name><name sortKey="Lacor, P" sort="Lacor, P" uniqKey="Lacor P" first="P." last="Lacor">P. Lacor</name><name sortKey="Thielemans, K" sort="Thielemans, K" uniqKey="Thielemans K" first="K." last="Thielemans">K. Thielemans</name></country><country name="Pays-Bas"><region name="Hollande-Méridionale"><name sortKey="De Goede, A L" sort="De Goede, A L" uniqKey="De Goede A" first="A. L." last="De Goede">A. L. De Goede</name></region><name sortKey="De Goede, A L" sort="De Goede, A L" uniqKey="De Goede A" first="A. L." last="De Goede">A. L. De Goede</name><name sortKey="De Goede, A L" sort="De Goede, A L" uniqKey="De Goede A" first="A. L." last="De Goede">A. L. De Goede</name><name sortKey="Gruters, R A" sort="Gruters, R A" uniqKey="Gruters R" first="R. A." last="Gruters">R. A. Gruters</name><name sortKey="Osterhaus, A D M E" sort="Osterhaus, A D M E" uniqKey="Osterhaus A" first="A. D. M. E." last="Osterhaus">A. D. M. E. Osterhaus</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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