- Autores: Abecasis AB, Theys K, Van Laethem K
- Ano de Publicação: 2015
- Journal: AIDS
- Link: https://insights.ovid.com/pubmed?pmid=25909833
Understanding the mechanisms and predictors of drug resistance development to HIV-1 antiretroviral therapy (ART) is a key challenge to further improve HIV-1 treatment strategies and prevent epidemic spread. The extensive genetic diversity characterizing the HIV-1 pandemic, classified into groups, subtypes and recombinants, has been shown to affect viral escape from drug-selective pressure and influence treatment decisions [1]. In previous issues of AIDS, Crawford and colleagues reported the selection of mutations E138A/G/K/Q upon treatment failure with first-generation non-nucleoside reverse transcriptase inhibitors (NNRTIs) efavirenz (EFV) or nevirapine (NVP) in patients infected with subtypes A1, D and recombinant form A2D [2,3]. Amino acid substitutions at polymorphic position E138 in the reverse transcriptase enzyme recently acquired clinical relevance by their association with reduced in-vitro activity and in-vivo response to second-generation NNRTIs etravirine and rilpivirine [4–7]. Crawford et al.[2] reported their findings as unique given that, in their dataset, mutations at E138 were selected in non-B subtype viruses and upon treatment exposure with first-generation NNRTIs.