Transmitted drug resistance to rilpivirine among antiretroviral-naive patients living with HIV from northern Poland.
PMID: 24746180
2014
Journal of the International AIDS Society
Abstract: RESULTS: IAS-USA RPV drug resistance mutations were found in 5.3% sequences, with E138A and E138G being the most common (3.7 and 0.8%, respectively), followed by K101E (0.4%) and Y181C (0.4%), with no significant differences in the frequency between subtype B and non-B clades.
Abstract: RPV-associated mutations were divided into RPV resistance mutations (K101E/P, E138A/G/K/Q/R, V179L, Y181C/I/V, Y188L, H221Y, F227C and M230I/L) according to the International AIDS Society-USA (I
E138A in HIV-1 reverse transcriptase is more common in subtype C than B: implications for rilpivirine use in resource-limited settings.
Abstract: E138A/K/Q in subtype C decreased RPV susceptibility 2.9-, 5.8-, and 5.4-fold, respectively.
Abstract: Taken together, these data suggest that E138A could impact treatment or prevention strategies that include RPV in geographic areas where subtype C infection is prevalent.
Abstract: We found that the E138A substitution occurs more frequently in subtype C (range: 5.9-7.5%) than B (range: 0-2.3%) sequences from both treatment-naive and -experienced individuals (p<0.01) in 4 independent genotype databases.
Introduction: Although RPV has been reported to have higher in vitro genetic barrier to resistance, at least 17 single substitutions in HIV-1 RT (L100I, K101E/P, E138A/G/K/Q/R,
Rilpivirine resistance and the dangerous liaisons with substitutions at position 184 among patients infected with HIV-1: analysis from a national drug-resistance database (ARCA).
Abstract: Among Italian patients the susceptibility to RPV is widespread since some severe substitutions (e.g., E138K are rare), whereas issues exist for others (i.e., E138A, Y181C) which are more frequent.
Abstract: In Italian HIV-positive HAART-naive patients, prevalence of the main RAMs for RPV is low except for E138A (present in 5.1% of subjects).
HIV-1 pol diversity among female bar and hotel workers in Northern Tanzania.
Real-life rilpivirine resistance and potential emergence of an E138A-positive HIV strain in north-eastern France.
PMID: 25006240
2014
The Journal of antimicrobial chemotherapy
Abstract: CONCLUSIONS: In our cohort of patients, we observed significantly increased resistance to rilpivirine, mostly because of the E138A mutation, probably due to an E138A strain circulating in newly diagnosed men who have sex with men.
Abstract: Seven viral strains from seven naive male patients positive for the E138A mutation appeared in the same cluster.
Abstract: The E138A mutation was the most frequent mutation associated with resistance to rilpivirine (P < 0.0001).
Abstract: The prevalence of the E138A mutation tended to increase over time, from 3.6% (2/55) during the first half of 2011 to 9.3% (4/43) during the first half of 2013 (P = 0.0614).
2014 Update of the drug resistance mutations in HIV-1.
Discussion: Cross-resistance studies with raltegravir- and elvitegravir-resistant viruses indicate that Q148H and G140S in combination with mutations L74I/M, E92Q, T97A, E138A/K, G140A, or N155H are associated with 5-fold to 20-fold reduced dolutegravir susceptibility and reduced virologic suppression in patients.
Discussion: Fifteen mutations have been associated with decreased rilpivirine susceptibility (K101E/P, E138A/G/K/Q/R, V179L, Y181C/I/V, H221Y, F227
Use of deep sequencing data for routine analysis of HIV resistance in newly diagnosed patients.
PMID: 25397493
2014
Journal of the International AIDS Society
Abstract: RESULTS: Using VisibleChek for analysis, we were able to describe the detection of any mutation using Sanger in 37/88 patients, with a total number of 50 Stanford >=5 mutations, K103N and E138A being the most prevalent (n=4).
Randomized trial of DRV/r or LPV/r QD monotherapy vs maintaining a PI/r-based antiretroviral regimen in persons with suppressed HIV replication.
PMID: 25397553
2014
Journal of the International AIDS Society
Abstract: A GRT was performed in 6/14 patients (one not amplifiable; four without mutations; one showed E138A).
Persistence of frequently transmitted drug-resistant HIV-1 variants can be explained by high viral replication capacity.