Method: RT-RAMs were identified and analyzed by using the Stanford Drug Resistance Database for V90I, A98G, L100I/V, K101E/P/Q/H/N, K103N/S/T/Q/E/H/R, V106A/M/I, V108I, E138A/K/Q/G/R, V179D/E/T/F/L, Y181C/I/V/S/F/G, M184I, Y188C/H/L/F, G190A/S/E/Q/C/V/T, H221Y,
Sub-Epidemics Explain Localized High Prevalence of Reduced Susceptibility to Rilpivirine in Treatment-Naive HIV-1-Infected Patients: Subtype and Geographic Compartmentalization of Baseline Resistance Mutations.
PMID: 26651266
2016
AIDS research and human retroviruses
Method: In addition, we defined a list of minor RPV-RAMs that have been observed in in vitro or in vivo selection studies and are included in one or more of clinically widely used genotypic resistance interpretation algorithms ANRS (V24), Rega (V9.1.0), and HIVdb (V7.0.1), encompassing V90I, A98G, L100I/V, K101H/Q/T, K103R/S, V106A/I, V108I, E138S, V179D/E/F/I/T, Y181F/G/S, Y188F, V189I, G190A/C/E/Q/S/T/V, and M230V
Comparison of genotypic and virtual phenotypic drug resistance interpretations with laboratory-based phenotypes among CRF01_AE and subtype B HIV-infected individuals.
Method: A NVP RAM was considered if at least one of the following genetic changes in reverse transcriptase was detected: A98G, K101E, K101H, K101P, K103N, V106A, V106M, V108I, Y181C, Y181V, Y188L and G190A.
Result: The mutations K101H, V106M, Y181V and Y188L were found in only one sample each (Fig 2).
Persistence of frequently transmitted drug-resistant HIV-1 variants can be explained by high viral replication capacity.
Transmitted drug resistance to rilpivirine among antiretroviral-naive patients living with HIV from northern Poland.
PMID: 24746180
2014
Journal of the International AIDS Society
Method: RPV resistance-associated mutations were divided into key resistance mutations (K101E/P, E138A/G/K/Q/R, V179L,Y181C/I/V, Y188L, H221Y, F227C and M230I/L) based on the IAS-USA drug resistance mutations list update 2013 and potential drug resistance mutations (L100I, K101H/T, E138S, V179F/D/G/T, G190A/E/S, F227L and M230V) based on the clinical trial and in
Non-nucleoside reverse transcriptase inhibitor (NNRTI) cross-resistance: implications for preclinical evaluation of novel NNRTIs and clinical genotypic resistance testing.
PMID: 23934770
2014
The Journal of antimicrobial chemotherapy
Abstract: K101H, E138G, V179F and M230L mutations, associated with reduced susceptibility to etravirine and rilpivirine, were also associated with reduced susceptibility to nevirapine and/or efavirenz.
Trends in Genotypic HIV-1 Antiretroviral Resistance between 2006 and 2012 in South African Patients Receiving First- and Second-Line Antiretroviral Treatment Regimens.
Method: The following non-polymorphic ARV-selected mutations were classified as drug resistance mutations (DRM): (i) the NRTI resistance mutations M41L, A62V, K65RN, D67NG, T69D, T69 insertions, T69 deletion, K70REGQ, L74VI, V75MT, F77L, Y115F, F116Y, Q151M, M184VI, L210W, T215YFSDCIV, and K219QENR; (ii) the
Effectiveness of first-line antiretroviral therapy and correlates of longitudinal changes in CD4 and viral load among HIV-infected children in Ghana.
HIV mutation literature information.
PMID: 
2016
PloS one
Browser Board
Co-occurred Entities
Filtrator
ViMRT