The Genotyping Resistance Profile of the Pol Gene Detected in Blood of Newly Diagnosed HIV-Positive Men Is Durably Archived in the Gut Whatever the Time of Initiation of cART.
Abstract: In 1 rilpivirine-treated patient, the M230I mutation was detected in PBMC.
Antiviral Activity of Bictegravir (GS-9883), a Novel Potent HIV-1 Integrase Strand Transfer Inhibitor with an Improved Resistance Profile.
PMID: 27645238
2016
Antimicrobial agents and chemotherapy
Result: Viral breakthrough with these agents contained HIV-RT mutations commonly associated with clinical resistance development (e.g., E138K and M230I for RPV, L100I for EFV, and M184I/V for FTC).
Distinctive Drug-resistant Mutation Profiles and Interpretations of HIV-1 Proviral DNA Revealed by Deep Sequencing in Reverse Transcriptase.
PMID: 27241734
2016
Biomedical and environmental sciences
Abstract: The mutations M184I and M230I were more prevalent in proviral DNA than in viral RNA (Fisher's exact test, P<0.05).
Usefulness of an HIV DNA resistance genotypic test in patients who are candidates for a switch to the rilpivirine/emtricitabine/tenofovir disoproxil fumarate combination.
PMID: 27231280
2016
The Journal of antimicrobial chemotherapy
Abstract: Rilpivirine/emtricitabine/tenofovir disoproxil fumarate RAMs studied were K65R, L100I, K101E/P, E138A/G/K/R/Q, V179L, Y181C/I/V, M184V/I, Y188L, H221Y, F227C and M230I/L in the RT.
Systematic review to determine the prevalence of transmitted drug resistance mutations to rilpivirine in HIV-infected treatment-naive persons.
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: Major RPV resistance-associated mutations (RPV-RAMs) were defined based on data from the clinical trials, phenotypic RPV resistance analyses, and package inserts: K101E/P, E138A/G/K/Q/R, V179L, Y181C/I/V, Y188L, H221Y, F227C, M230I/L, and the mutational combination of L100I+K103N.
Contribution of APOBEC3G/F activity to the development of low-abundance drug-resistant human immunodeficiency virus type 1 variants.
PMID: 26482266
2016
Clinical microbiology and infection
Abstract: APOBEC3G/F-associated E138K, M184I and M230I appeared within clonal sequences containing in-frame STOP codons in 2/3 (66%), 5/5 (100%) and 4/4 (100%) of the samples.
Abstract: In a large pan-European case-control study investigating the clinical relevance of pre-existing DRMVs using 454 pyrosequencing, the six most prevalent plasma DRMVs detected corresponded to G-to-A nucleotide mutations (V90I, V106I, V108I, E138K, M184I and M230I).
Abstract: Mutations E138K, M184I and M230I co-occurred in the same sequence as APOBEC3G/F signatures in 3/9 (33%), 5/11 (
2014 Update of the drug resistance mutations in HIV-1.
Discussion: Fifteen mutations have been associated with decreased rilpivirine susceptibility (K101E/P, E138A/G/K/Q/R, V179L, Y181C/I/V, H221Y, F227C, and M230I/L).
E138A in HIV-1 reverse transcriptase is more common in subtype C than B: implications for rilpivirine use in resource-limited settings.
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, V179L, Y181C/I/V, Y188L, H221Y, F227C, and M230I/L) have been associated with a decreased virologic response to this NNRTI.
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: 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 (IAS-USA) mutation list and variants potentially affecting RPV susceptibility (L100I, K101H/T, E138S, V179F/D/G/T, G190A/E/S, F227L and M230V) based on the
HIV mutation literature information.
PMID: 
2016
Intervirology
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