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

Photini Kiepiela, Alasdair J. Leslie, Isobella Honeyborne, Danni Ramduth, Christina Thobakgale, Senica Chetty, Prinisha Rathnavalu, Corey Moore, Katja J. Pfafferott, Louise Hilton, Peter Zimbwa, Sarah Moore, Todd Allen, Christian Brander, Marylyn M. Addo, Marcus Altfeld, Ian James, Simon Mallal, Michael Bunce, Linda D. Barber, James Szinger, Cheryl Day, Paul Klenerman, James Mullins, Bette Korber, Hoosen M. Coovadia, Bruce D. Walker and Philip J. R. Goulder ()
Additional contact information
Photini Kiepiela: University of KwaZuluNatal
Alasdair J. Leslie: Peter Medawar Building for Pathogen Research
Isobella Honeyborne: University of KwaZuluNatal
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
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
Hoosen M. Coovadia: University of KwaZuluNatal
Bruce D. Walker: University of KwaZuluNatal
Philip J. R. Goulder: University of KwaZuluNatal

Nature, 2004, vol. 432, issue 7018, 769-775

Abstract: 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

Date: 2004
References: Add references at CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/nature03113 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:432:y:2004:i:7018:d:10.1038_nature03113

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/nature03113

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().