Prevalence and patterns of HIV transmitted drug resistance in Guatemala.
PMID: 22358416
2011
Revista panamericana de salud publica
Abstract: Major NNRTI mutations such as K101E, K103N, and E138K showed higher frequencies than expected in ART-naive populations.
TMC278, a next-generation nonnucleoside reverse transcriptase inhibitor (NNRTI), active against wild-type and NNRTI-resistant HIV-1.
PMID: 19933797
2010
Antimicrobial agents and chemotherapy
Abstract: NNRTI RAMs emerging in HIV-1 under selective pressure from TMC278 included combinations of V90I, L100I, K101E, V106A/I, V108I, E138G/K/Q/R, V179F/I, Y181C/I, V189I, G190E, H221Y, F227C, and M230I/L.
IDX-899, an aryl phosphinate-indole non-nucleoside reverse transcriptase inhibitor for the potential treatment of HIV infection.
PMID: 20112173
2010
Current opinion in investigational drugs (London, England
Abstract: Two pathways of resistance have been identified for IDX-899 in vitro that include Glu138Lys and Val90Ile/Tyr181Cys mutations.
Impact of human leukocyte antigen-B*51-restricted cytotoxic T-lymphocyte pressure on mutation patterns of nonnucleoside reverse transcriptase inhibitor resistance.
Abstract: Computational analysis indicated that I135T and E138K cooperatively extend the gap between the binding site of reverse transcriptase and NNRTI.
Abstract: RESULTS: E138K emerged during the cultural passages of HIV-1I135V, HIV-1I135T, and HIV-1I135R, but not during the passages of HIV-1WT.
Abstract: The HIV-1I135L/E138K and HIV-1I135R/<
Abstract: The combination of I135T, the most frequent escape mutation, and E138K (HIV-1I135T/E138K) conferred significant resistance to efavirenz, nevirapine, and etravirine.
In vitro resistance development for RO-0335, a novel diphenylether nonnucleoside reverse transcriptase inhibitor.
Abstract: Two pathways to loss of susceptibility to RO-0335 were observed, containing patterns of amino acid changes at either V106I/A plus F227C (with additional contributions from A98G, V108I, E138K, M230L and P236L) or V106I/Y188L (with a potential contribution from L100I, E138K and Y181C).
The HIV-1 integrase mutations Y143C/R are an alternative pathway for resistance to Raltegravir and impact the enzyme functions.
Method: We followed-up the 50 mutations of resistance present at 32 positions: associated with in vitro or in vivo resistance to HIV-1 integrase inhibitors: H51Y, T66I/A/K, V72I, L74I/A/M, E92Q, T97A, T112I, F121Y, T125K, A128T, E138 K/A/D, G140R/C/H, Y143C/H/R, Q146K/P, S147G, Q148K/R/H, V151I, PMID: 20610719
2010
Journal of virology
1Abstract: Viruses containing G118R and E138K remained largely susceptible to both RAL and EVG, suggesting a unique interaction between this second-generation INSTI and the enzyme may be defined by these residues as a potential basis for the increased intrinsic affinity and longer ""off"" rate of MK-2048."
Abstract: Here, we report the identification of mutations (G118R and E138K) which confer resistance to MK-2048 and not to RAL or EVG.
Abstract: The subsequent selection of E138K partially restored replication capacity to approximately 13% of wt levels and increased resistance to MK-2048 to approximately 8-fold.
Effect of raltegravir resistance mutations in HIV-1 integrase on viral fitness.
PMID: 20634701
2010
Journal of acquired immune deficiency syndromes (1999)
Abstract: Fitness was partially restored by the presence of additional RAL resistance mutations at positions G140S and E92Q or E138K, respectively.
Result: By contrast, the E92Q/N155H mutant was fitter than the E138K/Q148H mutant both in the absence and presence of 5.0 microM RAL (Table 2).
Result: However, the E138K/Q148H mutant was less fit than G140S/Q148H in the absence and presence of drug.
Result: In the presence of raltegravir, the E138K/Q148H had a 3.0-fold relative fitness advantage over the
Distinct mutation pathways of non-subtype B HIV-1 during in vitro resistance selection with nonnucleoside reverse transcriptase inhibitors.
PMID: 20805392
2010
Antimicrobial agents and chemotherapy
Abstract: Y181C was the dominant mutation in the resistance selection with etravirine (ETV) in subtype A, and E138K/H221Y were the mutations detected in the breakthrough viruses from subtype C viruses with ETV.