The 118I reverse transcriptase mutation is the only independent genotypic predictor of virologic failure to a stavudine-containing salvage therapy in HIV-1-infected patients

Nicola Gianotti, Laura Galli, Enzo Boeri, Anna De Bona, Monica Guffanti, Anna Danise, Stefania Salpietro, Adriano Lazzarin, Antonella Castagna

Research output: Contribution to journalArticlepeer-review

Abstract

Patients infected with HIV-1 with more than 1000 HIV-1 RNA copies/mL, who were genotyped within 3 months before starting stavudine and treated for at least 3 months with a stable stavudine-containing highly active antiretroviral therapy, were selected from our database to identify the determinants of response to stavudine. Nonresponse was defined as a failure to achieve HIV-1 RNA level of less than 400 copies/mL or a reduction of more than 2 log10 by week 12. Univariate logistic analysis was used to elicit the failure-associated reverse transcriptase mutations (scored 1 to develop a genotype score). Eighty-one patients were eligible for the analysis, including 75 (93%) who previously received zidovudine. Thirty-five (43%) were nonresponders. Univariate logistic analysis revealed the following failure-associated mutations: 41L (P = 0.0001), 44D (P = 0.02), 118I (P = 0.0006), 184V (P = 0.04), 210W (P = 0.0004), and 215Y (P = 0.002) for a median stavudine score of 2. Failure was observed in 7 (18.9%) of 37 patients with a score less than 2, compared with 28 (63.6%) of 44 patients with a score of 2 or greater (P <0.0001). The multivariable analysis showed that the 118I mutation (P = 0.04) was the only independent genotypic predictor of failing on a stavudine-containing highly active antiretroviral therapy.

Original languageEnglish
Pages (from-to)447-452
Number of pages6
JournalJournal of Acquired Immune Deficiency Syndromes
Volume41
Issue number4
DOIs
Publication statusPublished - Apr 2006

Keywords

  • HAART
  • HIV-1 genotype
  • Stavudine
  • Virologic failure

ASJC Scopus subject areas

  • Immunology
  • Virology

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