Biochemical mechanism of clinical resistance to rilpivirine

Abstract

Background The introduction of HAART has significantly prolonged the life span of HIV-infected patients. However, the error-prone nature of HIV-1 reverse transcriptase (HIV-1 RT) results in the emergence of drug-resistant viruses and threatens the effectiveness of HAART. HIV-1 RT is a primary target of two classes of drugs: nucleoside reverse transcriptase inhibitors (NRTIs) and non-nucleoside reverse transcriptase inhibitors (NNRTIs). Recent phase III clinical trials have shown that two HIV-1 RT mutations, E138K and M184I, were the most frequent mutations found in patients that experienced virological failure during therapy that included rilpivirine (RPV), emtricitabine (FTC), and tenofovir (TDF).

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Cite this paper

@inproceedings{Singh2012BiochemicalMO, title={Biochemical mechanism of clinical resistance to rilpivirine}, author={Kamalendra Singh and Devendra Rai and Bechan Sharma and Eleftherios Michailidis and Emily M. Ryan and Kayla B. Matzek and Maxwell D. Leslie and Ariel N Hagedorn and Hongtao Xu and Mark A. Wainberg and Bruno Marchand and Stefan G. Sarafianos}, year={2012} }