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Common HIV-1 Peptide Variants Mediate Differential Binding of KIR3DL1 to HLA-Bw4 Molecules

  1. Author:
    Fadda, L.
    O'Connor, G. M.
    Kumar, S.
    Piechocka-Trocha, A.
    Gardiner, C. M.
    Carrington, M.
    McVicar, D. W.
    Altfeld, M.

  2. Author Address

    [Fadda, L; Kumar, S; Piechocka-Trocha, A; Carrington, M; Altfeld, M] Massachusetts Gen Hosp, Ragon Inst MGH MIT & Harvard, Charlestown, MA 02129 USA [O'Connor, GM; McVicar, DW] NCI, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21702 USA [Gardiner, CM] Trinity Coll Dublin, Sch Biochem & Immunol, Dublin, Ireland [Carrington, M] NCI, Canc & Inflammat Program, Expt Immunol Lab, SAIC Frederick Inc, Frederick, MD 21701 USA;Altfeld, M (reprint author), Massachusetts Gen Hosp, Ragon Inst MGH MIT & Harvard, Bldg 149,13th St, Charlestown, MA 02129 USA;maltfeld@partners.org
    1. Year: 2011
    2. Date: Jun
  2. Journal: Journal of Virology
    1. 85
    2. 12
    3. Pages: 5970-5974
  4. Type of Article: Article
  5. ISSN: 0022-538X
  1. Abstract:

    Epidemiological studies have shown the protective effect of KIR3DL1/HLA-Bw4 genotypes in human immunodeficiency virus type 1 (HIV-1) infection; however, the functional correlates for the protective effect remain unknown. We investigated whether human leukocyte antigen (HLA)-Bw4-presented HIV-1 peptides could affect the interaction between the inhibitory natural killer (NK) cell receptor KIR3DL1 and its ligand HLA-Bw4. Distinct HIV-1 epitopes differentially modulated the binding of KIR3DL1 to HLA-Bw4. Furthermore, cytotoxic T lymphocyte (CTL) escape mutations within the immunodominant HLA-B57 (Bw4)-restricted Gag epitope TSTLQEQIGW abrogated KIR3DL1 binding to HLA-B57, suggesting that sensing of CTL escape variants by NK cells can contribute to the protective effect of the KIR3DL1/HLA-Bw4 compound genotype.

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External Sources

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  2. DOI: 10.1128/jvi.00412-11
  3. View record in Web of Science®
  4. WOS: 000290756600025

Library Notes

  1. Fiscal Year: FY2010-2011
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