title: One-, two-, and three-class resistance among HIV-infected patients on antiretroviral therapy in private care clinics: Mumbai, India.
abstract: HIV-infected patients receiving antiretroviral (ARV) therapy (ART) in India are not all adequately virally suppressed. We analyzed ARV drug resistance in adults receiving ART in three private clinics in Mumbai, India. HIV viral load was measured in 200 patients with the Roche AMPLICOR HIV-1 Monitor Test, v1.5. HIV genotyping was performed with the ViroSeq HIV-1 Genotyping System for 61 participants who had HIV-1 RNA >1000 copies/ml. Genotyping results were obtained for 51 samples. The participants with resistance results were on ART for a median of 24 months and were on their current regimen for a median of 12 months (median CD4 cell count: 217 cells/mm(3); median HIV viral load: 28,200 copies/ml). ARV regimens included nonnucleoside reverse transcriptase inhibitor (NNRTI)-based regimens (n = 27), dual nucleoside reverse transcriptase inhibitors (NRTIs, n = 19), protease inhibitor (PI)-based regimens (n = 3), and other regimens (n = 2). Twenty-six participants (51.0%) were on their first ARV regimen and 24 (47%) reported >95% adherence. Forty-nine participants (96.1%) had resistance to at least one ARV drug; 47 (92.2%) had NRTI resistance, 32 (62.7%) had NNRTI resistance, and four (7.8%) had PI resistance. Thirty (58.8%) had two-class resistance and three (5.9%) had three-class resistance. Four (8%) had three or more resistance mutations associated with etravirine resistance and two (4%) had two mutations associated with reduced darunavir susceptibility. Almost all patients with HIV-1 RNA >1000 copies/ml had NRTI resistance and nearly two-thirds had NNRTI resistance; PI resistance was uncommon. Nearly 60% and 6% had two- and three-class resistance, respectively. This emphasizes the need for greater viral load and resistance monitoring, use of optimal ART combinations, and increased availability of second- and third-line agents for patients with ARV resistance.
authors.affiliation: Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA. agupta25@jhmi.edu
authors.forename: Amita
authors.initials: A
authors.lastname: Gupta
authors.forename: Dattaray G
authors.initials: DG
authors.lastname: Saple
authors.forename: Girish
authors.initials: G
authors.lastname: Nadkarni
authors.forename: Bijal
authors.initials: B
authors.lastname: Shah
authors.forename: Satish
authors.initials: S
authors.lastname: Vaidya
authors.forename: Nitin
authors.initials: N
authors.lastname: Hingankar
authors.forename: Devidas
authors.initials: D
authors.lastname: Chaturbhuj
authors.forename: Praveen
authors.initials: P
authors.lastname: Deshmukh
authors.forename: Louise
authors.initials: L
authors.lastname: Walshe
authors.forename: Sarah E
authors.initials: SE
authors.lastname: Hudelson
authors.forename: Maria
authors.initials: M
authors.lastname: James
authors.forename: Ramesh S
authors.initials: RS
authors.lastname: Paranjape
authors.forename: Susan H
authors.initials: SH
authors.lastname: Eshleman
authors.forename: Srikanth
authors.initials: S
authors.lastname: Tripathy
mesh_terms: D000328:Adult; D019943:Amino Acid Substitution / Q000235:genetics; D019380:Anti-HIV Agents / Q000494:pharmacology / Q000627:therapeutic use*; D023241:Antiretroviral Therapy, Highly Active; D018791:CD4 Lymphocyte Count; D024921:Drug Resistance, Multiple, Viral; D005260:Female; D005838:Genotype; D015658:HIV Infections / Q000188:drug therapy* / Q000821:virology*; D015497:HIV-1 / Q000187:drug effects* / Q000302:isolation & purification; D006801:Humans; D007194:India; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D012367:RNA, Viral / Q000235:genetics; D017422:Sequence Analysis, DNA; D019562:Viral Load
chemical_list: D019380:Anti-HIV Agents; D012367:RNA, Viral