Complex patterns of protease inhibitor resistance among antiretroviral treatment-experienced HIV-2 patients from Senegal: implications for second-line therapy.
PMID: 23571535
2013
Antimicrobial agents and chemotherapy
Abstract: Common protease substitutions included V10I, V47A, I54M, V71I, I82F, I84V, L90M, and L99F, and most patients harbored viruses containing multiple changes.
Abstract: In addition, the triple mutant that included I54M plus I84V plus L90M was resistant to all three PIs (31-, 10-, and 3.8-fold increases in the mean EC50 for darunavir, saquinavir, and lopinavir, respectively).
Abstract: Relative to wild-type HIV-2, the V47A mutant was resistant to lopinavir (6.3-fold increase in the mean 50% effectiv
Low frequency of genotypic resistance in HIV-1-infected patients failing an atazanavir-containing regimen: a clinical cohort study.
PMID: 23711895
2013
The Journal of antimicrobial chemotherapy
Result: The remaining 43 minor atazanavir mutations were either not detected in this dataset (L10C, K20V, E34Q, F53Y, I54L/M/T/A, A71L, G73C/T, V82F and
Discussion: Although there was a high frequency (7/39) of PI substitutions (including L33I/F and L90M, which we did not observe) in this subgroup, many patients were on NRTI-sparing dual-PI regimens and it is not possible to assess whether the substitutions observed were selected by atazanavir or by the other PI in the regimen.
Description of HIV-1 group M molecular epidemiology and drug resistance prevalence in Equatorial Guinea from migrants in Spain.
Result: The PI-resistance mutations found were M46L (4 cases), and L90M and I84V (3 cases each).
Table: L90M
Discussion: Thus, the PI-resistance mutation M46L, present in all subtype B viruses with TDR ( Table 5 ), was rare (<1%) among the subtype B-infected population living in Spain, where L90M was predominant.
Crystallographic study of multi-drug resistant HIV-1 protease lopinavir complex: mechanism of drug recognition and resistance.
PMID: 23792096
2013
Biochemical and biophysical research communications
Abstract: Mutations at residues 32I, L33F, 46I, 47A, I54V, V82A, I84V, and L90M
Introduction: Although drug resistance is relatively less likely to develop against LPV compared to other HIV-1 protease inhibitors, resistance mutations, including 32I, 47A, 46I, L33F, I54V, V82A, I84V, and L90M, or combinations among L76V, M46I, and V82A in the protease, and A431V in gag are responsible for reduced efficacy of LPV.
Trends in Genotypic HIV-1 Antiretroviral Resistance between 2006 and 2012 in South African Patients Receiving First- and Second-Line Antiretroviral Treatment Regimens.
Abstract: Within the viral protease, the major nelfinavir-resistance mutation L90M was found in one case.
Result: This case possessed HIV-1 RT mutations M41L, V90I, A98G, M184V and T215Y, and the major NFV-resistance mutation L90M in PR.
Table: L90M
Figure: *Major NFV-resistance mutation L90M was found in the protease in the case of KF307.
Simultaneous detection of major drug resistance mutations in the protease and reverse transcriptase genes for HIV-1 subtype C by use of a multiplex allele-specific assay.
PMID: 23985909
2013
Journal of clinical microbiology
Abstract: All the wild-type and mutant alleles were unequivocally distinguished with plasmid templates, and the limits of detection were 1.56% for K219Q and K219E, 3.13% for L76V, 6.25% for K65R, K70R, L74V, L100I, K103N, K103R, Q151M, Y181C, and I47V, and 12.5% for M41L, K101P, K101E, V106A, V106M, Y115F, M184V, PMID: 23991142
2013
PloS one
Abstract: RESULTS: At baseline, a prevalence of 3.6% (5/139) HIVDR was observed [protease inhibitors M46I (1/5), G73A (1/5), L90LM (1/5); nucleoside reverse transcriptase inhibitors: M184V (1/5), T215F (1/5); non-nucleoside reverse transcriptase inhibitors: K103N (1/5), Y181Y/C (2/5), M230ML (1/5)].
Result: Sequences from 5 patients were identified with drug resistance-associated mutations, giving a prevalence of 3.6% (5/139) HIVDR, among which 3 resistance mutations to protease inhibitors (M46I,
Prevalence and mutation patterns of HIV drug resistance from 2010 to 2011 among ART-failure individuals in the Yunnan Province, China.
Result: The other individual infected through heterosexual contact, had mutations of L90M and A71V and exhibited low-level resistance to atazanavir with ritonavir (ATV/r) and fosamprenavir with ritonavir (FPV/r), intermediate resistance to indinavir with ritonavir (IDV/r) and saquinavir with ritonavir (SQV/r), and high resistance to NFV/r.
HIV mutation literature information.
PMID: 
2013
Antimicrobial agents and chemotherapy
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