title: HIV-1 drug resistance in variants from the female genital tract and plasma.
abstract: BACKGROUND
  Human immunodeficiency virus type 1 (HIV-1) drug-resistance mutations may arise in a fraction of viral variants, and these variants may differ between compartments, including the genital tract and blood.
  
  
  METHODS
  We studied 14 women with detectable HIV-1 in both the genital tract and plasma despite antiretroviral treatment. We obtained HIV-1 RNA sequences from 280 unique viral variants and then determined the resistance genotype and the predicted phenotype (Virtual Phenotype; Virco BVBA) of each variant.
  
  
  RESULTS
  Eight patients (57%) displayed mutations conferring high-level HIV-1 drug resistance. Although we observed differences in specific mutations among viral variants, 13 of the 14 women showed highly concordant HIV-1 genotypic and predicted phenotypic resistance patterns in the 2 compartments. In 1 patient, resistance mutations appeared only in plasma; all variants in her genital tract, which displayed a low viral load, were susceptible.
  
  
  CONCLUSIONS
  These data suggest that, for the majority of women, determination of HIV-1 drug resistance in the plasma will approximate the drug-resistance pattern in the genital tract. Analysis of individual variants enabled us to identify minority species bearing distinctive linked mutations, which may serve as a source of novel resistance genotypes. These data are relevant to clinical management and the evolution of drug resistance.
authors.affiliation: Wadsworth Center, New York State Department of Health, Albany, NY 12208, USA.
authors.forename: Kimdar Sherefa
authors.initials: KS
authors.lastname: Kemal
authors.forename: Harold
authors.initials: H
authors.lastname: Burger
authors.forename: Douglas
authors.initials: D
authors.lastname: Mayers
authors.forename: Kathryn
authors.initials: K
authors.lastname: Anastos
authors.forename: Brian
authors.initials: B
authors.lastname: Foley
authors.forename: Christina
authors.initials: C
authors.lastname: Kitchen
authors.forename: Penelope
authors.initials: P
authors.lastname: Huggins
authors.forename: Tamara
authors.initials: T
authors.lastname: Schroeder
authors.forename: Gaston
authors.initials: G
authors.lastname: Picchio
authors.forename: Sara
authors.initials: S
authors.lastname: Back
authors.forename: Wei
authors.initials: W
authors.lastname: Gao
authors.forename: William A
authors.initials: WA
authors.lastname: Meyer
authors.forename: Barbara
authors.initials: B
authors.lastname: Weiser
mesh_terms: D000328:Adult; D019943:Amino Acid Substitution; D019380:Anti-HIV Agents / Q000494:pharmacology*; D024882:Drug Resistance, Viral / Q000235:genetics*; D005260:Female; D005836:Genitalia, Female / Q000821:virology*; D005838:Genotype; D015658:HIV Infections / Q000188:drug therapy / Q000821:virology*; D016333:HIV Protease / Q000235:genetics; D054303:HIV Reverse Transcriptase / Q000235:genetics; D015497:HIV-1 / Q000145:classification / Q000187:drug effects* / Q000235:genetics* / Q000302:isolation & purification; D006801:Humans; D008875:Middle Aged; D008969:Molecular Sequence Data; D020125:Mutation, Missense; D010802:Phylogeny; D010949:Plasma / Q000821:virology; D012367:RNA, Viral / Q000235:genetics; D017422:Sequence Analysis, DNA; D017385:Sequence Homology
chemical_list: D019380:Anti-HIV Agents; D012367:RNA, Viral; D054303:HIV Reverse Transcriptase; D016333:HIV Protease