Intensification of Background Antiretroviral Therapy with Abacavir during Low-Level Failure May Restore Optimal Suppression

Abstract

To investigate the antiviral activity of abacavir added to stable background therapy. Retrospective analysis. In 27 subjects with detectable plasma viraemia during stable treatment abacavir was added as the only agent. Patients were pre-treated for 180 weeks (mean) with regimens containing zidovudine (102 weeks) and lamivudine (88 weeks). Results were analysed in two groups: group 1, > 400 HIV RNA copies/ml; group 2, 25-399 copies/ml. In 7/13 group 1 patients genotypic resistance analysis was performed prior to abacavir. Median follow-up was 28 weeks, median HIV RNA load at baseline 2.48 log10 copies/ml (3.52 and 1.66 log10 copies/ml in groups 1 and 2, respectively). Plasma viraemia was reduced to less than 400 HIV RNA copies/ml in 2/13 subjects in group 1 and 11/11 in group 2 (week 24). Only one patient in group 1 responded transiently to less than 25 HIV RNA copies/ml. In contrast, 10/14 and 11/11 in group 2 reached values below this threshold at weeks 12 and 24, respectively. Overall, 7/13 group 1 patients were found with > or = 2 zidovudine resistance-associated mutations. The lamivudine resistance-associated mutation M184V was present in four of seven cases. All of these patients showed only a moderate and transient reduction of plasma viraemia (medium peak reduction of 0.73 log10 after 20 weeks). The addition of abacavir during low-level treatment failure may restore or achieve suppression to levels below the cut-off of the ultrasensitive PCR.