Extract

Global access to antiretroviral drugs has increased dramatically [1], and so have concerns regarding the development of drug resistance. The article in this issue of the Journal by Cozzi-Lepri et al [2] presents data detailing the rate of accumulation of thymidine analogue mutations (TAMs) in human immunodeficiency virus (HIV)–infected patients treated with antiretroviral drug combinations who continued to receive virologically failing regimens in a large European cohort (EuroSIDA) [3]. Prior studies from this cohort demonstrated a strong association between the presence of resistance at failure and the risk of clinical progression [4, 5]. This finding is in contrast to data revealing that continuing to receive a failing regimen might have immunological and virological benefits—namely, stable CD4 cell counts and less-fit viruses [6, 7]. According to the International AIDS Society–USA 2008 mutation list, TAMs are defined as the following specific mutations: M41L, D67N, K70R, L210W, T215Y/F, and K219Q/E [8]. The accumulation of TAMs is associated with cross-resistance to all nucleoside or nucleotide analogues, and the degree of resistance is dependent on both the specific mutations and their total number

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