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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26 November 2007
Commentary|
November 19 2007
Triple bypass: complicated paths to HIV escape
Andrew J. McMichael
Andrew J. McMichael
A.J. McMichael is at MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DS, UK
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Andrew J. McMichael
A.J. McMichael is at MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DS, UK
CORRESPONDENCE A.J.M.: [email protected]
Online ISSN: 1540-9538
Print ISSN: 0022-1007
The Rockefeller University Press
2007
J Exp Med (2007) 204 (12): 2785–2788.
Citation
Andrew J. McMichael; Triple bypass: complicated paths to HIV escape . J Exp Med 26 November 2007; 204 (12): 2785–2788. doi: https://doi.org/10.1084/jem.20072371
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