Dominant influence of HLA-B in mediating the potential co-evolution of HIV and HLA
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 cells 1 , 2 , 3 . HLA class I molecules present pathogen-derived peptides on the surface of infected cells for recognition by...
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| Published in | Nature (London) Vol. 432; no. 7018; pp. 769 - 775 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
09.12.2004
Nature Publishing Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| 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 cells
1
,
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 activity
4
,
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
< 0.0001 and
P
= 0.91, respectively). Moreover, substantially greater selection pressure is imposed on HIV-1 by HLA-B alleles than by HLA-A (4.4-fold,
P
= 0.0003). These data indicate that the principal focus of HIV-specific activity is at the HLA-B locus. Furthermore, HLA-B gene frequencies in the population are those likely to be most influenced by HIV disease, consistent with the observation that B alleles evolve more rapidly than A alleles
6
,
7
,
8
. The dominant involvement of HLA-B in influencing HIV disease outcome is of specific relevance to the direction of HIV research and to vaccine design. |
|---|---|
| AbstractList | 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 super(+) T cells. HLA class I molecules present pathogen-derived peptides on the surface of infected cells for recognition by CD8 super(+) 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 super(+) T-cell responses against human immunodeficiency virus (HIV-1), immune control of which is dependent upon virus-specific CD8 super(+) T-cell activity. In 375 HIV-1-infected study subjects from southern Africa, a significantly greater number of CD8 super(+) 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 < 0.0001 and P = 0.91, respectively). Moreover, substantially greater selection pressure is imposed on HIV-1 by HLA-B alleles than by HLA-A (4.4-fold, P = 0.0003). These data indicate that the principal focus of HIV-specific activity is at the HLA-B locus. Furthermore, HLA-B gene frequencies in the population are those likely to be most influenced by HIV disease, consistent with the observation that B alleles evolve more rapidly than A alleles. The dominant involvement of HLA-B in influencing HIV disease outcome is of specific relevance to the direction of HIV research and to vaccine design. 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 cells 1 , 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 activity 4 , 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 < 0.0001 and P = 0.91, respectively). Moreover, substantially greater selection pressure is imposed on HIV-1 by HLA-B alleles than by HLA-A (4.4-fold, P = 0.0003). These data indicate that the principal focus of HIV-specific activity is at the HLA-B locus. Furthermore, HLA-B gene frequencies in the population are those likely to be most influenced by HIV disease, consistent with the observation that B alleles evolve more rapidly than A alleles 6 , 7 , 8 . The dominant involvement of HLA-B in influencing HIV disease outcome is of specific relevance to the direction of HIV research and to vaccine design. 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 cells. 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 activity. 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 < 0.0001 and P = 0.91, respectively). Moreover, substantially greater selection pressure is imposed on HIV-1 by HLA-B alleles than by HLA-A (4.4-fold, P = 0.0003). These data indicate that the principal focus of HIV-specific activity is at the HLA-B locus. Furthermore, HLA-B gene frequencies in the population are those likely to be most influenced by HIV disease, consistent with the observation that B alleles evolve more rapidly than A alleles. The dominant involvement of HLA-B in influencing HIV disease outcome is of specific relevance to the direction of HIV research and to vaccine design.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 cells. 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 activity. 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 < 0.0001 and P = 0.91, respectively). Moreover, substantially greater selection pressure is imposed on HIV-1 by HLA-B alleles than by HLA-A (4.4-fold, P = 0.0003). These data indicate that the principal focus of HIV-specific activity is at the HLA-B locus. Furthermore, HLA-B gene frequencies in the population are those likely to be most influenced by HIV disease, consistent with the observation that B alleles evolve more rapidly than A alleles. The dominant involvement of HLA-B in influencing HIV disease outcome is of specific relevance to the direction of HIV research and to vaccine design. 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 cells. 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 activity. 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 < 0.0001 and P = 0.91, respectively). Moreover, substantially greater selection pressure is imposed on HIV-1 by HLA-B alleles than by HLA-A (4.4-fold, P = 0.0003). These data indicate that the principal focus of HIV-specific activity is at the HLA-B locus. Furthermore, HLA-B gene frequencies in the population are those likely to be most influenced by HIV disease, consistent with the observation that B alleles evolve more rapidly than A alleles. The dominant involvement of HLA-B in influencing HIV disease outcome is of specific relevance to the direction of HIV research and to vaccine design. 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 cells. 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 activity. 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 < 0.0001 and P = 0.91, respectively). Moreover, substantially greater selection pressure is imposed on HIV-1 by HLA-B alleles than by HLA-A (4.4-fold, P = 0.0003). These data indicate that the principal focus of HIV-specific activity is at the HLA-B locus. Furthermore, HLA-B gene frequencies in the population are those likely to be most influenced by HIV disease, consistent with the observation that B alleles evolve more rapidly than A alleles. The dominant involvement of HLA-B in influencing HIV disease outcome is of specific relevance to the direction of HIV research and to vaccine design. [PUBLICATION ABSTRACT] |
| Audience | Academic |
| Author | Goulder, Philip J. R. Honeyborne, Isobella Chetty, Senica Allen, Todd James, Ian Coovadia, Hoosen M. Brander, Christian Thobakgale, Christina Korber, Bette Walker, Bruce D. Klenerman, Paul Day, Cheryl Moore, Corey Ramduth, Danni Zimbwa, Peter Rathnavalu, Prinisha Kiepiela, Photini Addo, Marylyn M. Hilton, Louise Mullins, James Mallal, Simon Szinger, James Leslie, Alasdair J. Moore, Sarah Altfeld, Marcus Barber, Linda D. Pfafferott, Katja J. Bunce, Michael |
| Author_xml | – sequence: 1 givenname: Photini surname: Kiepiela fullname: Kiepiela, Photini organization: HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University of KwaZuluNatal – sequence: 2 givenname: Alasdair J. surname: Leslie fullname: Leslie, Alasdair J. organization: Department of Paediatrics, Nuffield Department of Medicine, Peter Medawar Building for Pathogen Research – sequence: 3 givenname: Isobella surname: Honeyborne fullname: Honeyborne, Isobella organization: HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University of KwaZuluNatal, Department of Paediatrics, Nuffield Department of Medicine, Peter Medawar Building for Pathogen Research – sequence: 4 givenname: Danni surname: Ramduth fullname: Ramduth, Danni organization: HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University of KwaZuluNatal – sequence: 5 givenname: Christina surname: Thobakgale fullname: Thobakgale, Christina organization: HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University of KwaZuluNatal – sequence: 6 givenname: Senica surname: Chetty fullname: Chetty, Senica organization: HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University of KwaZuluNatal – sequence: 7 givenname: Prinisha surname: Rathnavalu fullname: Rathnavalu, Prinisha organization: HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University of KwaZuluNatal – sequence: 8 givenname: Corey surname: Moore fullname: Moore, Corey organization: Centre for Clinical Immunology and Biomedical Statistics, Royal Perth Hospital and Murdoch University, Level 2 North Block, Royal Perth Hospital – sequence: 9 givenname: Katja J. surname: Pfafferott fullname: Pfafferott, Katja J. organization: Department of Paediatrics, Nuffield Department of Medicine, Peter Medawar Building for Pathogen Research – sequence: 10 givenname: Louise surname: Hilton fullname: Hilton, Louise organization: Department of Paediatrics, Nuffield Department of Medicine, Peter Medawar Building for Pathogen Research – sequence: 11 givenname: Peter surname: Zimbwa fullname: Zimbwa, Peter organization: Department of Paediatrics, Nuffield Department of Medicine, Peter Medawar Building for Pathogen Research – sequence: 12 givenname: Sarah surname: Moore fullname: Moore, Sarah organization: Department of Microbiology, University of Washington – sequence: 13 givenname: Todd surname: Allen fullname: Allen, Todd organization: Partners AIDS Research Center, Massachusetts General Hospital – sequence: 14 givenname: Christian surname: Brander fullname: Brander, Christian organization: Partners AIDS Research Center, Massachusetts General Hospital – sequence: 15 givenname: Marylyn M. surname: Addo fullname: Addo, Marylyn M. organization: Partners AIDS Research Center, Massachusetts General Hospital – sequence: 16 givenname: Marcus surname: Altfeld fullname: Altfeld, Marcus organization: Partners AIDS Research Center, Massachusetts General Hospital – sequence: 17 givenname: Ian surname: James fullname: James, Ian organization: Centre for Clinical Immunology and Biomedical Statistics, Royal Perth Hospital and Murdoch University, Level 2 North Block, Royal Perth Hospital – sequence: 18 givenname: Simon surname: Mallal fullname: Mallal, Simon organization: Centre for Clinical Immunology and Biomedical Statistics, Royal Perth Hospital and Murdoch University, Level 2 North Block, Royal Perth Hospital – sequence: 19 givenname: Michael surname: Bunce fullname: Bunce, Michael organization: Dynal Biotech Ltd – sequence: 20 givenname: Linda D. surname: Barber fullname: Barber, Linda D. organization: Anthony Nolan Research Institute, Royal Free Hospital – sequence: 21 givenname: James surname: Szinger fullname: Szinger, James organization: Santa Fe Institute, Los Alamos National Laboratory – sequence: 22 givenname: Cheryl surname: Day fullname: Day, Cheryl organization: Department of Paediatrics, Nuffield Department of Medicine, Peter Medawar Building for Pathogen Research – sequence: 23 givenname: Paul surname: Klenerman fullname: Klenerman, Paul organization: Department of Paediatrics, Nuffield Department of Medicine, Peter Medawar Building for Pathogen Research – sequence: 24 givenname: James surname: Mullins fullname: Mullins, James organization: Department of Microbiology, University of Washington – sequence: 25 givenname: Bette surname: Korber fullname: Korber, Bette organization: Santa Fe Institute, Los Alamos National Laboratory – sequence: 26 givenname: Hoosen M. surname: Coovadia fullname: Coovadia, Hoosen M. organization: HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University of KwaZuluNatal – sequence: 27 givenname: Bruce D. surname: Walker fullname: Walker, Bruce D. organization: HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University of KwaZuluNatal, Partners AIDS Research Center, Massachusetts General Hospital, Howard Hughes Medical Institute – sequence: 28 givenname: Philip J. R. surname: Goulder fullname: Goulder, Philip J. R. email: philip.goulder@ndm.ox.ac.uk organization: HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University of KwaZuluNatal, Department of Paediatrics, Nuffield Department of Medicine, Peter Medawar Building for Pathogen Research, Partners AIDS Research Center, Massachusetts General Hospital |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16328802$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/15592417$$D View this record in MEDLINE/PubMed |
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| Title | Dominant influence of HLA-B in mediating the potential co-evolution of HIV and HLA |
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