{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T16:30:53Z","timestamp":1790872253094,"version":"4.1.0"},"reference-count":29,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2012,4,15]],"date-time":"2012-04-15T00:00:00Z","timestamp":1334448000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["HIV Medicine"],"published-print":{"date-parts":[[2012,11]]},"abstract":"Objectives<\/jats:title>After structured treatment interruption (STI<\/jats:styled-content>) of treatment for HIV<\/jats:styled-content>\u20101, a fraction of patients maintain suppressed viral loads. Prospective identification of such patients might improve HIV<\/jats:styled-content>\u20101 treatment, if selected patients are offered STI<\/jats:styled-content>.<\/jats:p><\/jats:sec>Methods<\/jats:title>We analysed the effect of previously identified genetic modulators of HIV<\/jats:styled-content>\u20101 disease progression on patients\u2019 ability to suppress viral replication after STI<\/jats:styled-content>. Polymorphisms in the genes killer cell immunoglobulin\u2010like receptor 3DLI<\/jats:styled-content> (KIR3DL1<\/jats:styled-content><\/jats:italic>)\/KIR3DS1<\/jats:styled-content><\/jats:italic>, human leucocyte antigen B<\/jats:styled-content> (HLA<\/jats:styled-content>\u2010B<\/jats:styled-content><\/jats:italic>) and HLA Complex P5 (HCP5<\/jats:styled-content><\/jats:italic>), and a polymorphism affecting HLA<\/jats:styled-content>\u2010C<\/jats:styled-content> surface expression were analysed in 130 S<\/jats:styled-content>wiss HIV C<\/jats:styled-content>ohort S<\/jats:styled-content>tudy patients undergoing STI<\/jats:styled-content>. Genotypes were correlated with viral load levels after STI<\/jats:styled-content>.<\/jats:p><\/jats:sec>Results<\/jats:title>We observed a statistically significant reduction in viral load after STI<\/jats:styled-content> in carriers of HLA<\/jats:styled-content>\u2010B<\/jats:styled-content><\/jats:italic> alleles containing either the Bw480Thr<\/jats:styled-content> or the Bw480Ile<\/jats:styled-content> epitope (mean adjusted effect on post\u2010STI<\/jats:styled-content> viral load: \u22120.82 log HIV<\/jats:styled-content>\u20101 RNA<\/jats:styled-content> copies\/ml, P<\/jats:styled-content><\/jats:italic>\u2009<\u20090.001; and \u22121.12 log copies\/ml, P<\/jats:styled-content><\/jats:italic>\u2009<\u20090.001, respectively). No significant effects were detected for the other polymorphisms analysed. The likelihood of being able to control HIV<\/jats:styled-content>\u20101 replication using a prespecified cut\u2010off (viral load increase\u2009<\u20091000 copies\/ml) increased from 39% in Bw4<\/jats:styled-content>\u2010negative patients to 53% in patients carrying Bw4<\/jats:styled-content>\u201080Thr<\/jats:styled-content>, and to 65% in patients carrying Bw4<\/jats:styled-content>\u201080Ile (P<\/jats:styled-content><\/jats:italic>\u2009=\u20090.02).<\/jats:p><\/jats:sec>Conclusions<\/jats:title>These data establish a significant impact of HLA<\/jats:styled-content>\u2010Bw4<\/jats:styled-content> on the control of viral replication after STI<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/j.1468-1293.2012.01019.x","type":"journal-article","created":{"date-parts":[[2012,4,17]],"date-time":"2012-04-17T07:25:38Z","timestamp":1334647538000},"page":"589-595","source":"Crossref","is-referenced-by-count":3,"title":["HLA<\/scp>\u2010Bw4<\/scp> identifies a population of HIV<\/scp>\u2010infected patients with an increased capacity to control viral replication after structured treatment interruption"],"prefix":"10.1111","volume":"13","author":[{"given":"M","family":"Stern","sequence":"first","affiliation":[{"name":"Immunotherapy Laboratory Department of Biomedicine Outpatient Clinic University Hospital Basel Basel Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K","family":"Czaja","sequence":"additional","affiliation":[{"name":"Immunotherapy Laboratory Department of Biomedicine Outpatient Clinic University Hospital Basel Basel Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A","family":"Rauch","sequence":"additional","affiliation":[{"name":"University Clinic of Infectious Diseases University Hospital Bern and University of Bern Bern Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M","family":"Rickenbach","sequence":"additional","affiliation":[{"name":"Swiss HIV Cohort Study Data Center Lausanne University Lausanne Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H F","family":"G\u00fcnthard","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases and Hospital Epidemiology University Hospital Z\u00fcrich, University of Z\u00fcrich Z\u00fcrich Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M","family":"Battegay","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases University Hospital Basel Basel Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J","family":"Fellay","sequence":"additional","affiliation":[{"name":"Institute of Microbiology University Hospital Center Lausanne Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B","family":"Hirschel","sequence":"additional","affiliation":[{"name":"University Clinic of Infectious Diseases University Hospital of Geneva Geneva Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C","family":"Hess","sequence":"additional","affiliation":[{"name":"Immunobiology Laboratory Department of Biomedicine University Hospital Basel Basel Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"name":"the Swiss HIV Cohort Study 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