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De Novo generation of escape Variant-specific CD8+ T-Cell responses following Cytotoxic T-Lymphocyte escape in chronic Human Immunodeficiency Virus Type 1 Infection
Journal article   Open access   Peer reviewed

De Novo generation of escape Variant-specific CD8+ T-Cell responses following Cytotoxic T-Lymphocyte escape in chronic Human Immunodeficiency Virus Type 1 Infection

T.M. Allen, X.G. Yu, E.T. Kalife, L.L. Reyor, M. Lichterfeld, M. John, M. Cheng, R.L. Allgaier, S. Mui, N. Frahm, …
Journal of Virology, Vol.79(20), pp.12952-12960
2005
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Abstract

Human immunodeficiency virus type 1 (HIV-1) evades CD8+ T-cell responses through mutations within targeted epitopes, but little is known regarding its ability to generate de novo CD8+ T-cell responses to such mutants. Here we examined gamma interferon-positive, HIV-1-specific CD8+ T-cell responses and autologous viral sequences in an HIV-1-infected individual for more than 6 years following acute infection. Fourteen optimal HIV-1 T-cell epitopes were targeted by CD8+ T cells, four of which underwent mutation associated with dramatic loss of the original CD8+ response. However, following the G357S escape in the HLA-A11-restricted Gag349-359 epitope and the decline of wild-type-specific CD8+ T-cell responses, a novel CD8+ T-cell response equal in magnitude to the original response was generated against the variant epitope. CD8+ T cells targeting the variant epitope did not exhibit cross-reactivity against the wild-type epitope but rather utilized a distinct T-cell receptor Vβ repertoire. Additional studies of chronically HIV-1-infected individuals expressing HLA-A11 demonstrated that the majority of the subjects targeted the G357S escape variant of the Gag349-359 epitope, while the wild-type consensus sequence was significantly less frequently recognized. These data demonstrate that de novo responses against escape variants of CD8+ T-cell epitopes can be generated in chronic HIV-1 infection and provide the rationale for developing vaccines to induce CD8+ T-cell responses directed against both the wild-type and variant forms of CD8 epitopes to prevent the emergence of cytotoxic T-lymphocyte escape variants.

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Collaboration types
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Citation topics
1 Clinical & Life Sciences
1.66 HIV
1.66.46 HIV Pathogenesis
Web Of Science research areas
Virology
ESI research areas
Microbiology
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