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dc.contributor.authorWinchester, Robert
dc.contributor.authorPitt, Jane
dc.contributor.authorCharurat, Manhattan
dc.contributor.authorMagder, Laurence S.
dc.contributor.authorGoring, Harald H. H.
dc.contributor.authorLanday, Alan
dc.contributor.authorRead, Jennifer S.
dc.contributor.authorShearer, William T.
dc.contributor.authorHandelsman, Edward
dc.contributor.authorLuzuriaga, Katherine
dc.contributor.authorHillyer, George V.
dc.contributor.authorBlattner, William A.
dc.date2022-08-11T08:10:12.000
dc.date.accessioned2022-08-23T16:58:51Z
dc.date.available2022-08-23T16:58:51Z
dc.date.issued2004-06-01
dc.date.submitted2012-05-01
dc.identifier.citationJ Acquir Immune Defic Syndr. 2004 Jun 1;36(2):659-70.
dc.identifier.issn1525-4135 (Linking)
dc.identifier.pmid15167284
dc.identifier.urihttp://hdl.handle.net/20.500.14038/43456
dc.description.abstractThe 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.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=15167284&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://journals.lww.com/jaids/Fulltext/2004/06010/Mother_to_Child_Transmission_of_HIV_1__Strong.2.aspx#
dc.subjectAdolescent
dc.subjectAdult
dc.subjectAlleles
dc.subjectBase Sequence
dc.subjectCase-Control Studies
dc.subjectCohort Studies
dc.subjectDNA
dc.subjectFemale
dc.subjectGene Frequency
dc.subjectHIV Infections
dc.subject*HIV-1
dc.subjectHLA-B Antigens
dc.subjectHumans
dc.subjectImmunity, Innate
dc.subjectInfant, Newborn
dc.subjectInfectious Disease Transmission, Vertical
dc.subjectMale
dc.subjectModels, Molecular
dc.subjectPregnancy
dc.subjectProspective Studies
dc.subjectReceptors, Immunologic
dc.subjectReceptors, KIR
dc.subjectReceptors, KIR3DL1
dc.subjectImmunology and Infectious Disease
dc.subjectPediatrics
dc.titleMother-to-child transmission of HIV-1: strong association with certain maternal HLA-B alleles independent of viral load implicates innate immune mechanisms
dc.typeJournal Article
dc.source.journaltitleJournal of acquired immune deficiency syndromes (1999)
dc.source.volume36
dc.source.issue2
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/peds_immunology/39
dc.identifier.contextkey2814369
html.description.abstract<p>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.</p>
dc.identifier.submissionpathpeds_immunology/39
dc.contributor.departmentProgram in Molecular Medicine
dc.contributor.departmentDepartment of Pediatrics
dc.source.pages659-70


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