Biochemical mechanism of clinical resistance to rilpivirine


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).

Extracted Key Phrases

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} }