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• W2333701913 abstract "Because of the widespread use of zidovudine during the 1990s, the treatment history of many HIV-1-infected individuals relied on the first line of zidovudine-containing regimens followed by second lines of stavudine-containing regimens when virological failure occurred. After the removal of zidovudine pressure, some studies reported a slow rate of reversion of zidovudine resistance mutations, suggesting that these mutations have only a modest impact on viral replication in the absence of the drug [1–3], whereas others reported a fast reappearance of wild-type virus strains [4,5]. On the other hand, several recent studies have demonstrated that HIV-1 isolated from individuals failing stavudine-containing regimens often contain thymidine analogue mutations [6–8], which include M41L, D67N, K70R, L210W, T215Y/F and K219Q/E, previously associated only with zidovudine resistance. We have investigated whether the potential ongoing selective pressure exerted by a second line of stavudine-containing regimen might prevent the reversion of zidovudine-associated genotypic mutations in patients who have not been exposed to zidovudine for at least 3 years. Fourteen patients who had been treated with a first line of zidovudine-containing regimen for a median duration of 36 months (range 5–72 months) and had switched to a stavudine-containing regimen because of virological failure, were retrospectively included in the study. The median follow-up period after zidovudine discontinuation was 48 months (range 36–84 months). Patients were tested for HIV-1 drug resistance just before stopping their more recent zidovudine-containing regimen (baseline) and every year after zidovudine discontinuation (mean 3.5 follow-up samples per patient). Only patients with zidovudine-related genotypic resistance before the switch from zidovudine- to stavudine-containing regimen were selected. Reverse transcriptase (RT) genotype analysis was performed using an in-house procedure on the new eight capillary array sequencer CEQ 2000 System (Beckman Coulter Inc., Fullerton, CA, USA). Table 1 summarizes the treatment history, viral load and sequencing results for successive samples of these patients. The plasma viral load remained detectable during the whole treatment period: median (range) plasma viral loads at baseline and at the end of follow-up were 30 600 (2900–1 174 000) and 7782 (2253–1 021 260) HIV-1-RNA copies/ml, respectively.Table 1: Treatment history, viral load and sequencing results for successive samples of patients who switched from zidovudine- to stavudine-containing regimens. At baseline, the mean of mutations in the RT gene correlated with zidovudine-resistance was 3.4/RT gene. More than 3 years after the cessation of zidovudine therapy, reversal to wild-type amino acid for mutant codons in the RT gene did not occur under stavudine therapy (mean 3.4 zidovudine-mutations/RT gene at the end of follow-up). The main zidovudine resistance mutations: M41L, D67N, L210W, and T215Y/F were observed in eight, seven, eight, and 13 out of 14 baseline isolates, respectively. They persisted at the end of follow-up in all isolates but one (no. 9) with a disappearance of L210W and T215Y mutations within the second year after the discontinuation of zidovudine. These results are in discordance with reports of the fast reappearance of wild-type virus after stopping therapy [4,5] or switching nucleoside reverse transcriptase inhibitors to protease inhibitors [4]. On the other hand, previous studies have shown the persistence in the plasma of several mutations associated with zidovudine, 9 months after the discontinuation of zidovudine and switch to a triple combination regimen including stavudine, lamivudine and indinavir [3], or 14–15 months after the switch from zidovudine monotherapy to didanosine monotherapy in two patients [2]. Our results suggest that the switch from zidovudine to stavudine maintains a selective pressure that prevents the reversal of zidovudine-related mutations or the reappearence of virus with wild-type genotype. This switch does not allow the resensitizing of HIV to zidovudine, and leads to a genotypic resistance to stavudine and a decrease in susceptibility to abacavir [9]. This finding may have clinical implications when deciding on the optimal combination of nucleoside or non-nucleoside RT inhibitors as a component of multidrug regimens after first lines of therapy including zidovudine or stavudine, even more than 3 years after the discontinuation of zidovudine. Finally, these results offer further support to the concept that genotyping is necessary to select the components of antiretroviral regimens for patients experiencing treatment failure. Isabelle Pellegrin Isabelle Garrigue Anne Caumont Jean-Luc Pellegrin Patrick Merel Marie Hélène Schrive Pascal Bonot Hervé Fleury" @default.
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• W2333701913 date "2001-05-01" @default.
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• W2333701913 title "Persistence of zidovudine-resistance mutations in HIV-1 isolates from patients removed from zidovudine therapy for at least 3 years and switched to a stavudine-containing regimen" @default.
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• W2333701913 doi "https://doi.org/10.1097/00002030-200105250-00022" @default.
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