HIV-1 genotype and phenotype correlate with virological response to abacavir, amprenavir and efavirenz in treatment-experienced patients - PubMed (original) (raw)

Clinical Trial

. 2002 Feb 15;16(3):387-96.

doi: 10.1097/00002030-200202150-00010.

Mounir Ait-Khaled, Deborah A Thomas, Carol L Brosgart, Joseph J Eron Jr, Judith Feinberg, Timothy P Flanigan, Scott M Hammer, Peter W Kraus, Robert Murphy, Ramon Torres, Henry Masur; CNA2007 Study Team

Affiliations

Clinical Trial

HIV-1 genotype and phenotype correlate with virological response to abacavir, amprenavir and efavirenz in treatment-experienced patients

Judith Falloon et al. AIDS. 2002.

Abstract

Objective: To assess the safety and efficacy of three new drugs in patients with antiretroviral failure and to correlate retrospectively baseline factors with virological response.

Design and setting: Open-label, 48-week, single-arm, multi-center phase II trial conducted at nine US university or government clinics and private practices.

Patients and interventions: Patients with HIV-1 RNA > or =500 copies/ml despite > or =20 weeks of treatment with at least one protease inhibitor received abacavir 300 mg twice a day, amprenavir 1200 mg twice a day and efavirenz 600 mg once a day. Other antiretrovirals were prohibited until week 16 except for substitutions for possible abacavir hypersensitivity.

Main outcome measures: HIV RNA at weeks 16 and 48.

Results: A total of 101 highly treatment-experienced patients enrolled; 60 were naive to non-nucleoside analog reverse transcriptase inhibitors (NNRTI). HIV RNA < 400 copies/ml was attained in 25 out of 101 (25%) patients at 16 weeks (35% of NNRTI-naive and 10% of -experienced patients) and 23 (23%) patients at 48 weeks (33% of naive and 7% of experienced patients). CD4 cells increased by a median of 15 x 10(6) and 43 x 10(6) cells/l at weeks 16 and 48, respectively. Drug-related rash occurred in 50 out of 99 (51%) of patients, and 17 out of 99 (17%) permanently discontinued one or more drugs as a result. Lower baseline viral load, fewer NNRTI-related mutations, absence of decreased abacavir (> or =4-fold) and efavirenz (> or =10-fold) susceptibility, and greater number of drugs to which virus was susceptible were associated with virological response at week 16.

Conclusions: Abacavir, amprenavir and efavirenz durably reduced HIV RNA and increased CD4 cell counts in a subset of treatment-experienced adults. Baseline viral load and some genotypic and phenotypic markers of resistance correlated with HIV RNA response.

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