Method: RT mutations were identified from the International AIDS Society USA Drug (IAS-USA) mutation tables, spring 2008 (http://www.iasusa.org/resistance_mutations): M41L, K65R, D67N, insertion 69, K70R/E, L74I/V, L100I, K103N, V106A/M, V108I, Q151M, Y181I/C, M184V, Y188C/L, G190A/S, L210W, T215Y/F, 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.
Low frequency nonnucleoside reverse-transcriptase inhibitor-resistant variants contribute to failure of efavirenz-containing regimens in treatment- experienced patients.
PMID: 20102272
2010
The Journal of infectious diseases
Result: In subject 7N from the NNRTI-naive group (Fig 2A), a baseline sequence containing K103N clustered closely (bootstrap value 96) with sequences at failure containing K103N linked to Y188C or M230L.
Discussion: In one of 15 NNRTI-naive subjects (7N; figure 2A), an entry sequence containing K103N clustered closely with all the mutant sequences at failure containing K103N with M230L or Y181C.
Using of nevirapine is associated with intermediate and reduced response to etravirine among HIV-infected patients who experienced virologic failure in a resource-limited setting.
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 M230L nonnucleoside reverse transcriptase inhibitor resistance mutation in HIV-1 reverse transcriptase impairs enzymatic function and viral replicative capacity.
PMID: 20308384
2010
Antimicrobial agents and chemotherapy
Abstract: RT that contained M230L was also deficient in regard to each of minus-strand DNA synthesis, both DNA- and RNA-dependent polymerase activities, processivity, and RNase H activity,
Abstract: Phenotyping assays with TZM-bl cells confirmed that M230L conferred various degrees of resistance to each of the NNRTIs tested.
Abstract: Recombinant HIV-1 WT and M230L mutant RT enzymes were purified; and both biochemical and cell-based phenotypic assays confirmed that M230L conferred resistance to each of EFV, NVP, and ETR.
Abstract: Recombinant viruses containing M230L displayed an 8-fold decrease in RC compared to that of the parental wild-type (WT) virus.
The non-nucleoside reverse transcriptase inhibitor efavirenz stimulates replication of human immunodeficiency virus type 1 harboring certain non-nucleoside resistance mutations.
Method: M230L was introduced into wild-type pNL4-3 using the primers: 5'-CCT TTG GCT GGG TTA TGA ACT CCA TC-3' (forward) and 5'-GAT GGA GTT CAT AAC CCA GCC AAA GG-3' (reverse).
Result: There are no published reports of NNRTIs stimulating HIV-1 replication, although the M230L mutant was reported to display this property in presented but unpublished work (Huang W., Parkin N.T., Lie, Y.S., et al.
Result: We confirmed that the M230L mutant in an NL4-3 backbone does replicate better in the presence of low concentrations of EFV than in the absence of drug; the magnitude of EFV-dependent stimulation is similar to that observed with K101E+G190S, although the peak of growth stimulation occurred at a much lower EFV concentration than K101E+
Constrained patterns of covariation and clustering of HIV-1 non-nucleoside reverse transcriptase inhibitor resistance mutations.
PMID: 20462946
2010
The Journal of antimicrobial chemotherapy
Abstract: Of the 17 reported etravirine resistance-associated mutations (RAMs), Y181C/I/V, L100I, K101P and M230L were considered major based on published in vitro susceptibility data.
Abstract: RESULTS: Efavirenz preferentially selected for 16 mutations, including L100I (14% versus 0.1%, P < 0.001), K101P (3.3% versus 0.4%, P < 0.001) and M230L (2.8% versus 1.3%, P = 0.004), whereas nevirapine preferentially selected for 12 mutations, including Y181C/I/V (48% versus 6.9%, P < 0.001).
Method: Of these, L100I, K101P, Y181C/I/V and M230
Synthesis and Anti-HIV-1 Activity of a Novel Series of Aminoimidazole Analogs.
PMID: 20535242
2010
Letters in drug design & discovery
Introduction: Mutations associated with resistance to NNRTIs include L100I, K101E, K103N, V106A, V108I, V179D, Y181C, Y188C/L/H, G190A/E/S, M230L, P236L and Y318F.
Specific HIV-1 integrase polymorphisms change their prevalence in untreated versus antiretroviral-treated HIV-1-infected patients, all naive to integrase inhibitors.
PMID: 20817922
2010
The Journal of antimicrobial chemotherapy
Abstract: Similarly, V165I and G163R mutations were associated with the RT resistance mutations F227L and M230L, respectively, and the T206S polymorphism was associated with the RT resistance mutation L210W.
HIV mutation literature information.
PMID: 
2011
PloS one
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