Torsak BunupuradahJintanat AnanworanichPloenchan ChetchotisakdPacharee KantipongSupunnee JirajariyavejSunee SirivichayakulWarangkana MunsakulWisit PrasithsirikulSomnuek SungkanuparphChureeratana BowonwattanuwongVirat KlinbuayaemKathy PetoumenosBernard HirschelSorakij BhakeecheepKiat RuxrungthamThe HIV Netherlands Australia Thailand Research CollaborationUniversity of New South Wales (UNSW) AustraliaChulalongkorn UniversitySEARCHKhon Kaen UniversityChiangrai Prachanukroh HospitalTaksin HospitalVajira HospitalBamrasnaradura Infectious Disease InstituteMahidol UniversityChonburi Regional HospitalSanpatong HospitalUniversite de GeneveNational Health Security Office2018-05-032018-05-032011-11-03Antiviral Therapy. Vol.16, No.7 (2011), 1113-1121135965352-s2.0-80055099715https://repository.li.mahidol.ac.th/handle/20.500.14594/12225Background: We studied prevalence of etravirine (ETR) and rilpivirine (RPV) resistance in HIV-1 subtype CRF01-AE infection with first-line non-nucleoside reverse transcriptase inhibitor (NNRTI) failure. Methods: A total of 225 adults failing two nucleoside reverse transcriptase inhibitors (NRTIs) plus 1 NNRTI in Thailand with HIV RNA > 1,000 copies/ml were included. Genotypic resistance results and HIV-1 subtype were interpreted by Stanford DR database. ETR resistance was calculated by the new Monogram weighted score (Monogram WS; ≥4 indicating high-level ETR resistance) and by DUET weighted score (DUET WS; 2.5-3.5 and ≥4 resulted in intermediate and reduce ETR response, respectively). RPV resistance interpretation was based on previous reports. Results: Median (IQR) age was 38 (34-42) years, 41% were female and CDC A:B:C were 22%:21%:57%. HIV subtypes were 96% CRF01-AE and 4% B. Antiretrovirals at failure were lamivudine (100%), stavudine (93%), nevirapine (90%) and efavirenz (10%) with a median (IQR) duration of 3.4 (1.8-4.5) years. Median (IQR) CD4 + T-cell count and HIV RNA were 194 (121-280) cells/mm 3 and 4.1 (3.6-4.6) log 10 copies/ml, respectively. The common NNRTI mutations were Y181C (41%), G190A (22%) and K103N (19%). The proportion of patients with Monogram WS score ≥4 was 61.3%. By DUET WS, 49.8% and 7.5% of patients were scored 2.5-3.5 and ≥4, respectively. Only HIV RNA≥4 log 10 copies/ml at failure was associated with both Monogram WS≥4 (OR 2.3, 95% CI 1.3-3.9; P=0.003) and DUET WS≥2.5 (OR 1.9, 95% CI 1.1-3.3; P=0.02). The RVP resistance-associated mutations (RAMs) detected were K101P (1.8%), Y181I (2.7%) and Y181V (3.6%). All patients with RPV mutation had ETR resistance. No E138R/E138K mutations were detected. Conclusions: Approximately 60% of patients had highlevel ETR resistance. The role of ETR in second-line therapy is limited in late NNRTI failure settings. RVP RAMs were uncommon, but cross-resistance between ETR and RVP was high. ©2011 International Medical Press.Mahidol UniversityMedicinePharmacology, Toxicology and PharmaceuticsArticleSCOPUS10.3851/IMP1906