Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2510587 | Antiviral Research | 2010 | 6 Pages |
Abstract
Using quantitative deep HIV-1 sequencing in a subject who developed virological failure to deep salvage therapy with raltegravir, we found that most Q148R and N155H mutants detected at the time of virological failure originated from pre-existing minority Q148R and N155H variants through independent evolutionary clusters. Double 148R + N155H mutants were also detected in 1.7% of viruses at virological failure in association with E138K and/or G163R. Our findings illustrate the ability of HIV-1 to escape from suboptimal antiretroviral drug pressure through selection of pre-existing drug-resistant mutants, underscoring the importance of using fully active antiretroviral regimens to treat all HIV-1-infected subjects.
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Authors
Francisco M. Codoñer, Christian Pou, Alexander Thielen, Federico García, Rafael Delgado, David Dalmau, José Ramon Santos, Maria José Buzón, Javier Martínez-Picado, Miguel Álvarez-Tejado, Bonaventura Clotet, Lidia Ruiz, Roger Paredes,