OC-13 Efficacy of switching to bictegravir/emtricitabine/tenofovir alafenamide in people living with HIV with pre-existing NRTI resistances: a real-life experience

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Background We investigated the impact of pre-existing resistance associated mutations (RAMs) to nucleotide reverse transcriptase inhibitors (NRTI) on treatment outcomes among people living with HIV (PWH) receiving bictegravir/emtricitabine/tenofovir alafenamide (B/F/TAF) therapy in real-world clinical practice. Material and methods Single centre, retrospective review of all treatment-experienced adult PWH with pre-existing NRTI resistance, who switched to B/F/TAF since February 24, 2020. Demographics, clinical and laboratory history was extracted from our database, medical records and ARCA (table 1). Pre-existing RAMs (M184V, M41L, D67N, K65R, L210W, and T215Y/F) were determined through historical genotyping by Sanger sequencing. We assessed the virological and immunovirological response in PWH who completed 24 months of follow-up (M24). Results 52 PWH with pre-existing RAMs to NRTI were screened; 41/52 were included in the study (figure 1): 11 cases were excluded due to various reasons such as suspension of therapy before reaching 24 months (2/11), loss to follow-up (5/11), death before 24 months (2/11) or absence of required examinations at the time of the switch to B/F/TAF and/or at M24 (2/11). Among the 41 individuals, 28 had the M184V mutation, of whom 16 exhibiting only the M184V mutation (OM) and 11 showing the M184V mutation along with thymidine analog mutations (TAMs) (MT), while the remaining 11 had only TAMs (OT). Three individuals had the K65R mutation with one also having the M184V mutation. Pre-existing RAMs to NRTI did not influence treatment outcomes across the four groups (table 2). At M24, virological success (defined as HIV-RNA viral load < 50 copies/ml) was observed in 100% of cases in all groups (OM, MT and OT) and in the 3 individuals with K65R mutation. CD4+ cell count increased in 6 (37.5%), 9 (81.8%), and 6 (54.5%) individuals in the OM, MT and OT groups, respectively. Moreover, 32 out of 41 individuals (78.0%) achieved an increased CD4+/CD8+ ratio, with increases observed in 11 (68.8%) OM cases, 9 (81.8%) MT cases, 9 (81.8%) OT cases and in the 3 individuals with the K65R mutation. Conclusions B/F/TAF is an effective treatment option for virologically suppressed PWH even in those with the M184V mutation, as well as in individuals with other mutations linked to M184V, such as K65R or TAMs. These results underscore the efficacy of B/F/TAF in overcoming RAMs, thereby demonstrating its robust antiviral activity.

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