부산대학교 도서관

In view of the forthcoming long-acting antiretrovirals, measures should be taken to prevent the selection of HIV drug resistance mutations. All subjects who had been switched to boosted protease inhibitors plus maraviroc (bPIs/MVC) with baseline HIV-1 RNA >50 copies/mL between June, 2014, and April, 2015, were retrospectively evaluated. HIV-1 RNA, CD4+ T-cells, serum glucose, creatinine, ALT, and adverse events were controlled every 3 to 4 months. We retrospectively analyzed 44 patients: 18 were taking darunavir/ritonavir (DRV/r) and 26 atazanavir/ritonavir (ATV/r) once daily, plus MVC 300 mg once daily. Seven subjects were in CDC stage C. All had a follow-up of at least 24 weeks, 28 exceeded 48 weeks, and 21 exceeded 72 weeks. All had experienced at least 1 viral failure and had selected at least 1 resistance-associated mutation (RAM). At baseline, 38 had plasma HIV-1 RNA 50-499 copies/mL and 6 had ≥500. At week 24, none had viremia >500 and 30 (68.2%) had suppressed HIV-1 RNA below 50 copies/mL. Of the subgroup with 48 weeks' follow-up, 23 had HIV-1 RNA 50-499 copies/mL, 5 had ≥500, and 20/28 suppressed to <50 copies/mL. Of the longest observed subgroup (72 weeks), 17 had HIV-1 RNA 50-499 copies/mL, and 4 had ≥500 copies/mL and 15/21 (71.4%) suppressed to <50 copies/mL. This combination allowed fair suppression of viral replication, with minor genotypic evolution in 6 subjects, and seems to be a feasible strategy to prevent damaging future options.