{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,9,8]],"date-time":"2024-09-08T10:20:11Z","timestamp":1725790811292},"reference-count":24,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2013,11,12]],"date-time":"2013-11-12T00:00:00Z","timestamp":1384214400000},"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":[[2014,4]]},"abstract":"Objectives<\/jats:title>Although current guidelines recommend resistance testing prior to antiretroviral therapy (ART<\/jats:styled-content>) reinitiation after treatment interruptions, virological failure of first\u2010line ritonavir\u2010boosted, protease\u2010inhibitor (PI<\/jats:styled-content>\/r)\u2010containing ART<\/jats:styled-content> is associated with low emergent PI<\/jats:styled-content> resistance. In patients experiencing unscheduled treatment interruptions (UTrIs<\/jats:styled-content>) on ritonavir\u2010boosted atazanavir (ATV<\/jats:styled-content>\/r) ART<\/jats:styled-content> regimens, we hypothesized low emergence of PI<\/jats:styled-content> mutations conferring resistance to ATV<\/jats:styled-content>\/r.<\/jats:p><\/jats:sec>Methods<\/jats:title>In a retrospective assessment of HIV<\/jats:styled-content>\u2010infected patients initiating ATV<\/jats:styled-content>\/r\u2010containing ART<\/jats:styled-content>, using logistic regression we determined factors associated with UTrI<\/jats:styled-content>, the prevalence of emergent resistance mutations and virological response after ART<\/jats:styled-content> reinitiation.<\/jats:p><\/jats:sec>Results<\/jats:title>A total of 202 patients [median age 33 years (interquartile range (IQR<\/jats:styled-content>) 29\u201340 years); 52% female; median CD4<\/jats:styled-content> count 184 cells\/\u03bcL (IQR<\/jats:styled-content> 107\u2013280 cells\/\u03bcL); median HIV RNA<\/jats:styled-content> 4.6 log10<\/jats:sub> HIV<\/jats:styled-content>\u20101 RNA<\/jats:styled-content> copies\/mL (IQR<\/jats:styled-content> 3.2\u20135.1 copies\/mL)] initiated ATV<\/jats:styled-content>\/r between 2004 and 2009; 80 (43%) were ART<\/jats:styled-content> na\u00efve. One hundred and ten patients (55%) underwent 195 UTrIs<\/jats:styled-content> after a median (IQR<\/jats:styled-content>) 25 (10\u201352) weeks on ART<\/jats:styled-content>, with a median (IQR<\/jats:styled-content>) UTrI<\/jats:styled-content> duration of 10 (3\u201331) weeks. Fifty\u2010four of 110 patients (49%) underwent more than one UTrI<\/jats:styled-content>. The commonest reasons for UTrI<\/jats:styled-content> were nonadherence (52.7%) and drug intolerance (20%). Baseline HIV RNA<\/jats:styled-content> >\u2009100\u2009000 copies\\mL [odds ratio (OR<\/jats:styled-content>) 3.6; 95% confidence interval (CI<\/jats:styled-content>) 1.3\u20139.95] and being HCV<\/jats:styled-content> positive, an injecting drug user or on methadone (OR<\/jats:styled-content> 2.4; 95% CI<\/jats:styled-content> 1.3\u20134.4) were independently associated with UTrI<\/jats:styled-content>. In 39 patients with at least two resistance assays during UTrIs<\/jats:styled-content>, 72 new mutations emerged; four nucleoside reverse transcriptase inhibitor (NRTI<\/jats:styled-content>), two nonnucleoside reverse transcriptase inhibitor (NNRTI<\/jats:styled-content>) and 66 protease inhibitor (PI<\/jats:styled-content>) resistance mutations. All emergent PI<\/jats:styled-content> resistance mutations were minor mutations. At least 65% of patients were re\u2010suppressed on ATV<\/jats:styled-content>\/r reinitiation.<\/jats:p><\/jats:sec>Conclusions<\/jats:title>In this PI<\/jats:styled-content>\u2010treated cohort, UTrIs<\/jats:styled-content> are common. All emergent PI<\/jats:styled-content> resistance mutations were minor and ATV<\/jats:styled-content>\/r retained activity and efficacy when reintroduced, even after several UTrIs<\/jats:styled-content>, raising questions regarding the need for routine genotypic resistance assays in PI<\/jats:styled-content>\/r\u2010treated patients prior to ART<\/jats:styled-content> reinitiation after UTrI<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/hiv.12107","type":"journal-article","created":{"date-parts":[[2013,11,12]],"date-time":"2013-11-12T08:11:46Z","timestamp":1384243906000},"page":"224-232","source":"Crossref","is-referenced-by-count":6,"title":["Characterization of associations and development of atazanavir resistance after unplanned treatment interruptions"],"prefix":"10.1111","volume":"15","author":[{"given":"W","family":"Tinago","sequence":"first","affiliation":[{"name":"HIV Molecular Research Group School of Medicine and Medical Science University College Dublin Dublin Ireland"},{"name":"Department of Community Medicine College of Health Sciences University of Zimbabwe Harare Zimbabwe"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"JA","family":"O'Halloran","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases Mater Misericordiae University Hospital Dublin Ireland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"RM","family":"O'Halloran","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases Mater Misericordiae University Hospital Dublin Ireland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A","family":"Macken","sequence":"additional","affiliation":[{"name":"HIV Molecular Research Group School of Medicine and Medical Science University College Dublin Dublin Ireland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"JS","family":"Lambert","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases Mater Misericordiae University Hospital Dublin Ireland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"GJ","family":"Sheehan","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases Mater Misericordiae University Hospital Dublin Ireland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"PWG","family":"Mallon","sequence":"additional","affiliation":[{"name":"HIV Molecular Research Group School of Medicine and Medical Science University College Dublin Dublin Ireland"},{"name":"Department of Infectious Diseases Mater Misericordiae University Hospital Dublin Ireland"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2013,11,12]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1097\/QAI.0b013e31819675e9"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1097\/QAI.0b013e3181c79ab0"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.2165\/00003088-200544100-00003"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1097\/01.aids.0000216371.76689.63"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1097\/QAI.0b013e3181c990bf"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(08)61081-8"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1086\/656363"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1097\/00126334-200408150-00003"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-154-7-201104050-00316"},{"key":"e_1_2_6_11_1","doi-asserted-by":"publisher","DOI":"10.1021\/ci900012k"},{"key":"e_1_2_6_12_1","first-page":"99","article-title":"Role of atazanavir in the treatment of HIV infection","volume":"5","author":"Rivas P","year":"2009","journal-title":"Ther Clin Risk Manag"},{"key":"e_1_2_6_13_1","doi-asserted-by":"publisher","DOI":"10.3851\/IMP1719"},{"key":"e_1_2_6_14_1","doi-asserted-by":"publisher","DOI":"10.3851\/IMP1745"},{"key":"e_1_2_6_15_1","first-page":"77","article-title":"European HIV drug resistance guidelines panel. 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