9th Annual Conference Of The British HIV Association [BHIVA] 24 – 26 April 2003, University of Manchester Institute of Science & Technology (UMIST) Manchester

[AUTHOR(S):] C McDonald¹, S Kegg², R Kulasegaram³, M Smith¹, C Taylor¹, P Easterbrook¹, B Peters³, P Hay² and AM Geretti^1
1 King's College Hospital, ² St Thomas's Hospital and ³ St George's Hospital, London, UK

BHIVA Conf 2003 Apr 24-26;9:O12

OBJECTIVE: To determine the impact of previously detected nucleoside reverse transcriptase inhibitor (NRTI) resistance on the maintenance of virological control in antiretroviral-experienced patients switching from stavudine to tenofovir with a viral load (VL) of <50 copies/ml.

METHODS: Retrospective and prospective observational cohort study. Eligible patients (n=25) had been on two or more previous antiretroviral regimens and had a stable viral load of <50 copies/ml at the time of switching. Genotypic resistance was determined in plasma samples by either the TruGene Assay (Visible Genetics) or in-house sequencing.

RESULTS: The patients had a mean of 2.5 previous antiretroviral regimens and 5.1 years of NRTI therapy; 21/25 (84%) had one or more mutations at RT codons 41, 67, 70, 210, 215 and 219 (thymidine analogue mutations). None had K65R. Reasons for switching included lipoatrophy in 18, peripheral neuropathy in two, hepatic steatosis in one and unstated in four patients. At week 24, 20/25 patients (80%) had VL <50 copies/ml, including 10 with previous M41L plus two other TAMs or L210W in any context; all 20 were on protease inhibitor (PI)- based therapy with nelfinavir, ritonavir/saquinavir or ritonavir/lopinavir. One was lost to follow-up. Four (16%) had a virological rebound >400 copies/ml (two on NNRTI- and two on PI-based therapy). At rebound, resistance testing showed re-emergence of mutations at codons 41, 70, 210, 215 and 219. Two patients had K65R.

CONCLUSIONS: In NRTI-experienced patients switching from stavudine to tenofovir with a PI-based regimen, virological control was maintained despite a history of resistance mutations known to affect tenofovir.

PRESENTING AUTHOR: C McDonald

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