Result: G190A, E138A/G) were found concurrently both in viral RNA and proviral DNA, in two patients resistance mutations (M46I and G190E) were detected only in viral RNA, and in five patients archived transmitted drug resistance mutations (M230I, G73S, M184I, M46I, and A62V) in proviral DNA were identified.
Table: E138G
Selective resistance profiles emerging in patient-derived clinical isolates with cabotegravir, bictegravir, dolutegravir, and elvitegravir.
Introduction: One patient acquired virus with the Q148R mutation, conferring phenotypic resistance to RAL, EVG and CAB, in association with the K103N, E138G, and K238T, conferring cross-resistance to non-nucleoside RT inhibitors (NNRTIs).
Frequent cross-resistance to rilpivirine among subtype C HIV-1 from first-line antiretroviral therapy failures in South Africa.
Figure: FC resistance was evaluated based on the contribution of the number of RPV-associated mutations (L100I, K101E/P, E138A/G/K/Q/R, V179L, Y181C/I/V, Y188L, H221Y, F227C and M230I/L) per sample with and without K103N.
Potential for immune-driven viral polymorphisms to compromise antiretroviral-based preexposure prophylaxis for prevention of HIV-1 infection.
Discussion: Reverse transcriptase-E138K is the most commonly identified mutation upon virologic failure of rilpivirine-containing ART, conferring two to three-fold decreased susceptibility to this drug when present alone; E138A and E138G confer the same level of rilpivirine resistance as E138K.
Discussion: Using large global datasets of linked HIV/HLA genotypes, we demonstrate that E138X variants (most commonly E138A, E138G, or E138K) naturally occur in persons expressing HLA-B*18 allele in the majority of global regions and in most major HIV-1 group M subtypes and CRFs.
Week 48 resistance analysis of Elvitegravir/Cobicistat/Emtricitabine/Tenofovir DF versus Atazanavir + Ritonavir + Emtricitabine/Tenofovir DF in HIV-1 infected women (WAVES study GS-US-236-0128).
Abstract: A62V, V90I, K103N, or E138A/G/K/Q; 68-82%) demonstrated virologic suppression at week 48, with no resistance development except for one patient with M184V and pre-existing K103N in the ATV + RTV + FTC/TDF group.
The infection staging and profile of genotypic distribution and drug resistance mutation among the human immunodeficiency virus-1 infected blood donors from five Chinese blood centers, 2012-2014.
Result: 31 specific DRMs were identified from 27 samples with DRMs distributing as: 1) 74.2% (23/31) DRMs were on nonnucleoside reverse transcriptase inhibitors (NNRTIs) as: V179E/D (n = 16), K238N (n = 2), E138A/G (n = 4) and G190E (n = 1).
Result: For example, 16 of 27 donors showed PLLR (or above) to NNRTI due to V179D/E mutations; three donors with mutations of E138A were found to have PLLR to etravirine (ETR) and low-level resistance (LLR) to rilpivirine (RPV); specimen CQ12003214 was identified to have PLLR to five PIs and intermediate resistance (IR) to nelfinavir (NFV) caused by
Etravirine combined with antiretrovirals other than darunavir/ritonavir for HIV-1-infected, treatment-experienced adults: Week 48 results of a phase IV trial.
Discussion: Using NGS, a total of 13 patients presented the E138A mutation over the 20% threshold and 10 additional patients presented E138 mutants as low-abundance variants <20%, including E138A, E138K and E138G.
Prevalence of HIV-1 Subtypes and Antiretroviral Drug Resistance Mutations in Nepal.
HIV mutation literature information.
PMID: 
2018
PloS one
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