Abstract
Objective
To investigate the antiviral activity of abacavir added to stable background therapy. Design: Retrospective analysis.
Materials and Methods
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.
Results
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 ≥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).
Conclusions
The addition of abacavir during low-level treatment failure may restore or achieve suppression to levels below the cut-off of the ultrasensitive PCR.