Intensification of background antiretroviral therapy with abacavir during low-level failure may restore optimal suppression

Objective: To investigate the antiviral activity of abacavir added to stabl e background therapy. Design: Retrospective analysis. Materials and Methods: In 27 subjects with detectable plasma viraemia durin g 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 2.4 8 log(10) copies/ml (3.52 and 1.66 log(10) copies/ml in groups 1 and 2, res pectively). 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 patien t in group 1 responded transiently to less than 25 HIV RNA copies/ml. In co ntrast, 10/14 and 11/11 in group 2 reached values below this threshold at w eeks 12 and 24, respectively. Overall, 7/13 group 1 patients were found wit h greater than or equal to 2 zidovudine resistance-associated mutations. Th e lamivudine resistance-associated mutation M184V was present in four of se ven cases. All of these patients showed only a moderate and transient reduc tion of plasma viraemia (medium peak reduction of 0.73 log(10) after 20 wee ks). Conclusions: The addition of abacavir during low-level treatment failure ma y restore or achieve suppression to levels below the cut-off of the ultrase nsitive PCR.