{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,28]],"date-time":"2026-01-28T04:23:41Z","timestamp":1769574221917,"version":"3.49.0"},"reference-count":25,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2017,2,20]],"date-time":"2017-02-20T00:00:00Z","timestamp":1487548800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Plan Nacional I+D+I","award":["RD12\/0017\/0031"],"award-info":[{"award-number":["RD12\/0017\/0031"]}]},{"name":"Plan Nacional I+D+I","award":["PI11\/0870"],"award-info":[{"award-number":["PI11\/0870"]}]},{"name":"ISCIII-Subdirecci\u00f3n General de Evaluaci\u00f3n and European Regional Development Fund"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["HIV Medicine"],"published-print":{"date-parts":[[2017,9]]},"abstract":"<jats:sec><jats:title>Objectives<\/jats:title><jats:p>The objective of this study was to seek correlates of immune protection in <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content> infection. We sought to elucidate the association between the presence of human leucocyte antigen (<jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>) alleles, as well as killer immunoglobulin receptor (<jats:styled-content style=\"fixed-case\">KIR<\/jats:styled-content>) genotypes, and the susceptibility to <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content> infection in a Spanish cohort of <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>\u2010exposed seronegative (<jats:styled-content style=\"fixed-case\">HESN<\/jats:styled-content>) individuals.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>A total of 152 individuals were evaluated: 29 <jats:styled-content style=\"fixed-case\">HESN<\/jats:styled-content> individuals in stable heterosexual relationships with an <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>\u2010infected partner admitting high\u2010risk sexual intercourse for at least 12 months prior to inclusion in the study, 61 <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>\u2010infected patients and 62 healthy controls. <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content> class I and <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> alleles and <jats:styled-content style=\"fixed-case\">KIR<\/jats:styled-content> genotypes were assessed in genomic <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> from all individuals in the study by polymerase chain reaction\u2212sequence\u2010specific oligonucleotide (<jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">SSO<\/jats:styled-content>) using bead array technology.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">HESN<\/jats:styled-content> individuals showed a higher prevalence of <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010A3 (62%) and <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010B44 (83%) supertypes compared with <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>\u2010infected individuals (42% and 66%, respectively). Regarding specific <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content> alleles, <jats:styled-content style=\"fixed-case\">HESN<\/jats:styled-content> individuals had a higher prevalence of <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010A*33:01, <jats:styled-content style=\"fixed-case\">DRB<\/jats:styled-content>1*04 and <jats:styled-content style=\"fixed-case\">DQB<\/jats:styled-content>1*03:02 alleles (14%, 34% and 31%, respectively) and a lower prevalence of the <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010A*02:01 allele (27%) than <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>\u2010infected patients (3%, 15%, 11% and 52%, respectively; <jats:italic>P<\/jats:italic> &lt; 0.05). Interestingly, in a multivariate analysis, only the presence of <jats:styled-content style=\"fixed-case\">DQB<\/jats:styled-content>1*03:02 and the absence of A*02:01 alleles were independently associated with <jats:styled-content style=\"fixed-case\">HESN<\/jats:styled-content> status [odds ratio (<jats:styled-content style=\"fixed-case\">OR<\/jats:styled-content>) 3.4 (95% confidence interval (<jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>) 1.1\u201310.5) and 0.4 (95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>: 0.1\u20130.9), respectively; <jats:italic>P<\/jats:italic> &lt; 0.05]. No <jats:styled-content style=\"fixed-case\">KIR<\/jats:styled-content> genotype was associated with susceptibility to <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content> infection.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Our data showed that the presence of the <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content> class <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> allele <jats:styled-content style=\"fixed-case\">DQB<\/jats:styled-content>1*03:02 was a correlate of immune protection against <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content> infection, while the presence of the <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content> class I allele A*02:01 was associated with being infected with <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/hiv.12494","type":"journal-article","created":{"date-parts":[[2017,2,20]],"date-time":"2017-02-20T10:36:46Z","timestamp":1487587006000},"page":"587-594","source":"Crossref","is-referenced-by-count":16,"title":["Human leucocyte antigen (<scp>HLA<\/scp>)\u2010<scp>DQB<\/scp>1*03:02 and <scp>HLA<\/scp>\u2010A*02:01 have opposite patterns in their effects on susceptibility to <scp>HIV<\/scp> infection"],"prefix":"10.1111","volume":"18","author":[{"given":"N","family":"Rall\u00f3n","sequence":"first","affiliation":[{"name":"Jim\u00e9nez D\u00edaz Foundation\u2010Health Research Institute UAM Madrid Spain"},{"name":"Rey Juan Carlos University Hospital M\u00f3stoles Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C","family":"Restrepo","sequence":"additional","affiliation":[{"name":"Jim\u00e9nez D\u00edaz Foundation\u2010Health Research Institute UAM Madrid Spain"},{"name":"Rey Juan Carlos University Hospital M\u00f3stoles Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"JL","family":"Vicario","sequence":"additional","affiliation":[{"name":"Histocompatibility Lab. Community Transfusion Center of Madrid Madrid Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J","family":"del Romero","sequence":"additional","affiliation":[{"name":"Madrid Sanitary Center Sandoval Madrid Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C","family":"Rodr\u00edguez","sequence":"additional","affiliation":[{"name":"Madrid Sanitary Center Sandoval Madrid Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J","family":"Garc\u00eda\u2010Samaniego","sequence":"additional","affiliation":[{"name":"Carlos III\u2010La Paz University Hospital Madrid Spain"},{"name":"CIBERehd Madrid Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M","family":"Garc\u00eda","sequence":"additional","affiliation":[{"name":"Jim\u00e9nez D\u00edaz Foundation\u2010Health Research Institute UAM Madrid Spain"},{"name":"Rey Juan Carlos University Hospital M\u00f3stoles 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