title: HIV-1 subtypes in Luxembourg, 1983-2000.
abstract: OBJECTIVE
  To study the prevalence of HIV-1 subtypes in Luxembourg between 1983 and 2000. To compare the drug susceptibility of non-B and B clade viruses and the prevalence of resistance-associated mutations and polymorphisms before antiretroviral treatment.
  
  
  METHODS
  A retrospective study on plasma samples of HIV-infected patients registered at the National Service of Infectious Diseases, Luxembourg, between 1983 and 2000.
  
  
  METHODS
  Genotyping was performed by sequencing of the reverse transcriptase (RT) and protease coding region of the pol gene. Drug susceptibility was assessed in a recombinant virus assay.
  
  
  RESULTS
  A total of 20.1% of the HIV-positive patients were infected with non-B subtypes, and since 1990 the proportion of non-B viruses has increased ninefold. Eleven out of 14 F1 subtypes occurred in patients native to Luxembourg. Major resistance mutations related to protease inhibitors (PI), nucleoside reverse transcriptase inhibitors (NRTI) and non-nucleoside reverse transcriptase inhibitors (NNRTI) occurred in less than 3% of treatment-naive viruses; however, 87% of the viruses had at least one PI-associated mutation. Natural polymorphism of the protease and RT coding region was observed more frequently among non-B than B viruses. Significantly more B viruses displayed resistance to the tested PI, NRTI and NNRTI (P = 0.044).
  
  
  CONCLUSIONS
  The proportion of non-B viruses has increased dramatically since 1990. Non-B subtypes showed no decreased susceptibility to antiretroviral drugs, but displayed minor mutations and polymorphisms at higher frequency in their protease and RT coding region. In contrast, a significantly higher proportion of B viruses showed resistance to a range of antiretroviral drugs.
authors.affiliation: Laboratoire de Rétrovirologie, Centre de Recherche Public-Santé, 4 rue Barblé, L-1210 Luxembourg, Luxembourg. deroo.s@retrovirology.lu
authors.forename: Sabrina
authors.initials: S
authors.lastname: Deroo
authors.forename: Isabelle
authors.initials: I
authors.lastname: Robert
authors.forename: Elodie
authors.initials: E
authors.lastname: Fontaine
authors.forename: Christine
authors.initials: C
authors.lastname: Lambert
authors.forename: Jean-Marc
authors.initials: JM
authors.lastname: Plesséria
authors.forename: Vic
authors.initials: V
authors.lastname: Arendt
authors.forename: Thérèse
authors.initials: T
authors.lastname: Staub
authors.forename: Robert
authors.initials: R
authors.lastname: Hemmer
authors.forename: François
authors.initials: F
authors.lastname: Schneider
authors.forename: Jean-Claude
authors.initials: JC
authors.lastname: Schmit
mesh_terms: D000328:Adult; D000368:Aged; D023241:Antiretroviral Therapy, Highly Active / Q000379:methods; D024882:Drug Resistance, Viral; D005260:Female; D005838:Genotype; D015658:HIV Infections / Q000188:drug therapy / Q000453:epidemiology* / Q000235:genetics; D016333:HIV Protease / Q000235:genetics; D017320:HIV Protease Inhibitors; D054303:HIV Reverse Transcriptase / Q000235:genetics; D015497:HIV-1 / Q000235:genetics*; D006801:Humans; D008189:Luxembourg / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D009154:Mutation / Q000235:genetics; D011110:Polymorphism, Genetic; D015995:Prevalence; D012189:Retrospective Studies; D018894:Reverse Transcriptase Inhibitors
chemical_list: D017320:HIV Protease Inhibitors; D018894:Reverse Transcriptase Inhibitors; D054303:HIV Reverse Transcriptase; D016333:HIV Protease