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Dominant influence of HLA-B in mediating the potential co-evolution of HIV and HLA

Author

Listed:
  • Photini Kiepiela

    (University of KwaZuluNatal)

  • Alasdair J. Leslie

    (Peter Medawar Building for Pathogen Research)

  • Isobella Honeyborne

    (University of KwaZuluNatal
    Peter Medawar Building for Pathogen Research)

  • Danni Ramduth

    (University of KwaZuluNatal)

  • Christina Thobakgale

    (University of KwaZuluNatal)

  • Senica Chetty

    (University of KwaZuluNatal)

  • Prinisha Rathnavalu

    (University of KwaZuluNatal)

  • Corey Moore

    (Royal Perth Hospital)

  • Katja J. Pfafferott

    (Peter Medawar Building for Pathogen Research)

  • Louise Hilton

    (Peter Medawar Building for Pathogen Research)

  • Peter Zimbwa

    (Peter Medawar Building for Pathogen Research)

  • Sarah Moore

    (University of Washington)

  • Todd Allen

    (Massachusetts General Hospital)

  • Christian Brander

    (Massachusetts General Hospital)

  • Marylyn M. Addo

    (Massachusetts General Hospital)

  • Marcus Altfeld

    (Massachusetts General Hospital)

  • Ian James

    (Royal Perth Hospital)

  • Simon Mallal

    (Royal Perth Hospital)

  • Michael Bunce

    (Dynal Biotech Ltd)

  • Linda D. Barber

    (Royal Free Hospital)

  • James Szinger

    (Santa Fe Institute
    Los Alamos National Laboratory)

  • Cheryl Day

    (Peter Medawar Building for Pathogen Research)

  • Paul Klenerman

    (Peter Medawar Building for Pathogen Research)

  • James Mullins

    (University of Washington)

  • Bette Korber

    (Santa Fe Institute
    Los Alamos National Laboratory)

  • Hoosen M. Coovadia

    (University of KwaZuluNatal)

  • Bruce D. Walker

    (University of KwaZuluNatal
    Massachusetts General Hospital
    Howard Hughes Medical Institute)

  • Philip J. R. Goulder

    (University of KwaZuluNatal
    Peter Medawar Building for Pathogen Research
    Massachusetts General Hospital)

Abstract

The extreme polymorphism in the human leukocyte antigen (HLA) class I region of the human genome is suggested to provide an advantage in pathogen defence mediated by CD8+ T cells1,2,3. HLA class I molecules present pathogen-derived peptides on the surface of infected cells for recognition by CD8+ T cells. However, the relative contributions of HLA-A and -B alleles have not been evaluated. We performed a comprehensive analysis of the class I restricted CD8+ T-cell responses against human immunodeficiency virus (HIV-1), immune control of which is dependent upon virus-specific CD8+ T-cell activity4,5. In 375 HIV-1-infected study subjects from southern Africa, a significantly greater number of CD8+ T-cell responses are HLA-B-restricted, compared to HLA-A (2.5-fold; P = 0.0033). Here we show that variation in viral set-point, in absolute CD4 count and, by inference, in rate of disease progression in the cohort, is strongly associated with particular HLA-B but not HLA-A allele expression (P

Suggested Citation

  • Photini Kiepiela & Alasdair J. Leslie & Isobella Honeyborne & Danni Ramduth & Christina Thobakgale & Senica Chetty & Prinisha Rathnavalu & Corey Moore & Katja J. Pfafferott & Louise Hilton & Peter Zim, 2004. "Dominant influence of HLA-B in mediating the potential co-evolution of HIV and HLA," Nature, Nature, vol. 432(7018), pages 769-775, December.
    • Handle: RePEc:nat:nature:v:432:y:2004:i:7018:d:10.1038_nature03113
    DOI: 10.1038/nature03113
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    Cited by:

    1. Wayne Delport & Konrad Scheffler & Cathal Seoighe, 2008. "Frequent Toggling between Alternative Amino Acids Is Driven by Selection in HIV-1," PLOS Pathogens, Public Library of Science, vol. 4(12), pages 1-13, December.

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