Integrase inhibitor (INI) genotypic resistance in treatment-naive and raltegravir-experienced patients infected with diverse HIV-1 clades.
PMID: 26311843
2015
The Journal of antimicrobial chemotherapy
Method: Dolutegravir resistance categories were as follows: (i) no resistance, absence of Q148H/R/K; (ii) low-level resistance, Q148H/R/K in the absence of G140S/A/C, L74I and E138A/K/T; (iii) intermediate-level resistance, Q148H/R/K with one of the mutations G140S/A/C, L74I or E138A/K/T; and (iv) high-level resistance, Q148H/R/K with two or three of the mutations G140S/A/C, L74I and E138A/K/T.
Comparison of 454 Ultra-Deep Sequencing and Allele-Specific Real-Time PCR with Regard to the Detection of Emerging Drug-Resistant Minor HIV-1 Variants after Antiretroviral Prophylaxis for Vertical Transmission.
Result: Twenty-eight NVP-selected mutations (V90I, K101E, K103N/R, V106A/I/M, V108I, E138A/G/K/R, Y181C, Y188C, G190A or P225H) were detected in 19 samples at levels of 1.1% to 99.1%.
Table: E138A
HIV Drug Resistance Surveillance in Honduras after a Decade of Widespread Antiretroviral Therapy.
Result: E138GAR mutations, conferring DR to rilpivirine and etravirine were also highly prevalent (4.7%), causing higher PDR estimations when using the Stanford DR definition (Table 3).
Lack of integrase inhibitors associated resistance mutations among HIV-1C isolates.
PMID: 26626277
2015
Journal of translational medicine
Discussion: This includes T66IAK, E92Q, F121Y, G140SA, Y143HCR, Q146P, S147G, Q148KHR, and N155HS; (2) minor INI-resistance mutations were defined as non-polymorphic or minimally polymorphic mutations that reduce INI susceptibility H51Y, L74 M, T97A, E138AK, S153Y,
Sensitive testing of plasma HIV-1 RNA and Sanger sequencing of cellular HIV-1 DNA for the detection of drug resistance prior to starting first-line antiretroviral therapy with etravirine or efavirenz.
PMID: 24284781
2014
The Journal of antimicrobial chemotherapy
Abstract: Conversely, 11/79 (13.9%) patients randomized to etravirine had one polymorphic RAM from the etravirine score in baseline plasma (V90I, V106I or E138A), without any impact on virological outcomes.
Competitive fitness assays indicate that the E138A substitution in HIV-1 reverse transcriptase decreases in vitro susceptibility to emtricitabine.
PMID: 24419343
2014
Antimicrobial agents and chemotherapy
Abstract: The E138A substitution, typically associated with decreased virologic responses to ETV- and RPV-containing regimens, confers a clear fitness advantage to the virus in the presence of FTC and decreases FTC susceptibility 4.7-fold.
Incidence of transmitted antiretroviral drug resistance in treatment-naive HIV-1-infected persons in a large South Central United States clinic.
Discussion: Results from the HIV-1 drug resistance mutation research by the International AIDS Society-USA (updated in March 2013) have revealed that PI resistance mutation sites are L10I, K20M, V32I, M36I, M46I/L, I47V/A, I50V, Q58E, A71V, G73S, V82A/F/T, I84V, L89V,L90M; NRTIs resistance mutations are M41L, A62V, PMID: 24698843
2014
AIDS (London, England)
Abstract: Three resistance mutations with more than 20% prevalence were detected solely by UDS: A98S (23%), E138A (21%) and V179I (25%).
Prevalence in the USA of rilpivirine resistance-associated mutations in clinical samples and effects on phenotypic susceptibility to rilpivirine and etravirine.
Abstract: METHODS: In total, 15,991 samples submitted to Monogram Biosciences (South San Francisco, CA, USA) for routine resistance testing between January 2010 and June 2011 were assessed for the presence of known rilpivirine RAMs K101E/P, E138A/G/K/Q/R, V179L, Y181C/I/V, Y188L, H221Y, F227C and M230I/L; non-nucleoside reverse transcriptase inhibitor (NNRTI) RAMs K103N, L100I and L100I+K103N; and the
HIV mutation literature information.
PMID: 
2015
The Journal of antimicrobial chemotherapy
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