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8th Annual Conference Of The British HIV Association [BHIVA]19 – 21 April 2002, University of York, York |
[AUTHOR(S):] A Winston, S Mandalia, D Pillay, B Gazzard, A Pozniak
Chelsea & Westminster Hospital, London
BHIVA Conf 2002 Apr 19-21;8:O12
BACKGROUND: The K65R mutation in HIV-1 reverse transcriptase is associated with reduced susceptibility to abacavir and tenofovir. We established its prevalence within a large clinical database, and investigated correlations with other resistance-associated mutations and antiretroviral history.
METHODS: Genotypes from the Chelsea & Westminster Hospital resistance database (up to October 2001) were analysed. Data from patients who had received tenofovir were excluded.
RESULTS: K65R was identified in viruses from 17 of 999 patients tested (1.70%). Nine of the 17 were receiving abacavir (group 1). In comparing group 1 with 177 patients failing treatment on abacavir without the K65R mutation (group 2), no differences were observed for time on abacavir, time on antiretrovirals or number of concurrent drugs. Current thymidine analogue treatment was more common in group 2 (68% versus 32%; P<0.05), as was the prevalence of two or more thymidine analogue-associated resistance mutations (48% versus 11%; P<0.05).
CONCLUSIONS: The presence of K65R is associated with prior abacavir use. Although rare, it is preferentially selected within non-thymidine analogue-containing regimens, compared with concurrent zidovudine or stavudine use, which is associated with emergence of thymidine analogue mutations. Both genetic routes taken may compromise both abacavir and tenofovir activity.
PRESENTING AUTHOR: A Winston
020419
O12
Copyright © 2002 - British HIV Association (BHIVA) Reproduction of this abstract (other than one copy for personal reference) must be cleared through the BHIVA Organising Secretariat 1 Mountview Court, 310 Friern Barnet Lane, London N20 0LD