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    Mother-to-child transmission of HIV-1: strong association with certain maternal HLA-B alleles independent of viral load implicates innate immune mechanisms

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    Authors
    Winchester, Robert
    Pitt, Jane
    Charurat, Manhattan
    Magder, Laurence S.
    Goring, Harald H. H.
    Landay, Alan
    Read, Jennifer S.
    Shearer, William T.
    Handelsman, Edward
    Luzuriaga, Katherine
    Hillyer, George V.
    Blattner, William A.
    Show allShow less
    UMass Chan Affiliations
    Program in Molecular Medicine
    Department of Pediatrics
    Document Type
    Journal Article
    Publication Date
    2004-06-01
    Keywords
    Adolescent
    Adult
    Alleles
    Base Sequence
    Case-Control Studies
    Cohort Studies
    DNA
    Female
    Gene Frequency
    HIV Infections
    *HIV-1
    HLA-B Antigens
    Humans
    Immunity, Innate
    Infant, Newborn
    Infectious Disease Transmission, Vertical
    Male
    Models, Molecular
    Pregnancy
    Prospective Studies
    Receptors, Immunologic
    Receptors, KIR
    Receptors, KIR3DL1
    Immunology and Infectious Disease
    Pediatrics
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    Link to Full Text
    http://journals.lww.com/jaids/Fulltext/2004/06010/Mother_to_Child_Transmission_of_HIV_1__Strong.2.aspx#
    Abstract
    The transmission of HIV-1 from mother to child during pregnancy is unlike other types of HIV-1 transmission because the child shares major histocompatibility complex (MHC) genes with the mother during a time while the mother is induced to tolerate the paternally derived fetal MHC molecules, in part through natural killer (NK) recognition of MHC polymorphisms. The relevance of these immune mechanisms to HIV-1 transmission was assessed by determining the HLA-B alleles of mother and infant. Almost half (48%) of mothers who transmitted with low viral loads had HLA-B*1302, B*3501, B*3503, B*4402, or B*5001 alleles, compared with 8% of nontransmitting mothers (P=0.001). Conversely, 25% of mothers who did not transmit despite high viral loads had B*4901 and B*5301, vs. 5% of transmitting mothers (P=0.003), a pattern of allelic involvement distinct from that influencing HIV-1 infection outcome. The infant's HLA-B alleles did not appear associated with transmission risk. The HLA-B*4901 and B*5301 alleles that were protective in the mother both differed respectively from the otherwise identical susceptibility alleles, B*5001 and B*3501, by 5 amino acids encoding the ligand for the KIR3DL1 NK receptor. These results suggest that the probable molecular basis of the observed association involves definition of the maternal NK recognition repertoire by engagement of NK receptors with polymorphic ligands encoded by maternal HLA-B alleles, and that the placenta is the likely site of the effect that appears to protect against transmission of maternal HIV-1 through interrelating adaptive and innate immune recognition.
    Source
    J Acquir Immune Defic Syndr. 2004 Jun 1;36(2):659-70.
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/43456
    PubMed ID
    15167284
    Related Resources
    Link to Article in PubMed
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    UMass Chan Faculty and Researcher Publications

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