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Triple bypass: complicated paths to HIV escape

Human immunodeficiency virus (HIV) type 1 is highly efficient at evading immune responses and persisting, ultimately causing fatal immunodeficiency in some patients. Mutation in the epitopes recognized by cytolytic CD8(+) T cells (CTLs) is one such escape process. A new study now shows that one HIV-...

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Detalles Bibliográficos
Autor principal: McMichael, Andrew J.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118526/
https://www.ncbi.nlm.nih.gov/pubmed/18025124
http://dx.doi.org/10.1084/jem.20072371
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author McMichael, Andrew J.
author_facet McMichael, Andrew J.
author_sort McMichael, Andrew J.
collection PubMed
description Human immunodeficiency virus (HIV) type 1 is highly efficient at evading immune responses and persisting, ultimately causing fatal immunodeficiency in some patients. Mutation in the epitopes recognized by cytolytic CD8(+) T cells (CTLs) is one such escape process. A new study now shows that one HIV-1 escape mutation may also result in impaired dendritic cell (DC) activity, possibly impairing later T cell responses to the same and other epitopes. The new data complete our understanding of the mechanisms by which the CTL response to an immunodominant gag epitope presented by human histocompatibility leukocyte antigen (HLA)-B27 is evaded. The complexity of the full escape helps to explain why patients with this HLA type progress to AIDS more slowly than average.
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spelling pubmed-21185262008-05-26 Triple bypass: complicated paths to HIV escape McMichael, Andrew J. J Exp Med Commentaries Human immunodeficiency virus (HIV) type 1 is highly efficient at evading immune responses and persisting, ultimately causing fatal immunodeficiency in some patients. Mutation in the epitopes recognized by cytolytic CD8(+) T cells (CTLs) is one such escape process. A new study now shows that one HIV-1 escape mutation may also result in impaired dendritic cell (DC) activity, possibly impairing later T cell responses to the same and other epitopes. The new data complete our understanding of the mechanisms by which the CTL response to an immunodominant gag epitope presented by human histocompatibility leukocyte antigen (HLA)-B27 is evaded. The complexity of the full escape helps to explain why patients with this HLA type progress to AIDS more slowly than average. The Rockefeller University Press 2007-11-26 /pmc/articles/PMC2118526/ /pubmed/18025124 http://dx.doi.org/10.1084/jem.20072371 Text en Copyright © 2007, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Commentaries
McMichael, Andrew J.
Triple bypass: complicated paths to HIV escape
title Triple bypass: complicated paths to HIV escape
title_full Triple bypass: complicated paths to HIV escape
title_fullStr Triple bypass: complicated paths to HIV escape
title_full_unstemmed Triple bypass: complicated paths to HIV escape
title_short Triple bypass: complicated paths to HIV escape
title_sort triple bypass: complicated paths to hiv escape
topic Commentaries
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118526/
https://www.ncbi.nlm.nih.gov/pubmed/18025124
http://dx.doi.org/10.1084/jem.20072371
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