Transmitted drug resistance and phylogenetic relationships among acute and early HIV-1-infected individuals in New York City.
PMID: 22592583
2012
Journal of acquired immune deficiency syndromes (1999)
4Method: ARV resistance was defined by mutations at the following positions: M41L, A62V, K65R, D67N, T69ins, K70R, L74VI, Y115F, F116Y, Q151M, M184VI, T210W, T215YF and K219QE for
Result: Mutations M41L (3.7%), T215Y/F/S/D/C/E (4.0%), K103N/S (4.7%) and L90M were most prevalent.
HIV-1 protease with 20 mutations exhibits extreme resistance to clinical inhibitors through coordinated structural rearrangements.
Result: Also, in vitro studies show that combining the two mutations D30N and L90M results in PR that exhibits high levels of resistance to nelfinavir.
Result: Analysis of mutation patterns in eight thousand and sixty virus isolates reveals that N88D is positively associated with D30N, and facilitates the occurrence of major resistance mutations D30N and L90M resulting in multidrug resistance.
Result: Six other mutations Q7K, L10F, L33F, I54L, N88D and L90M are located in the second shell with direct influence on the inhibitor-interacting r
Energetic basis for drug resistance of HIV-1 protease mutants against amprenavir.
PMID: 22350569
2012
Journal of computer-aided molecular design
Abstract: For the L90M mutant, a rise in the van der Waals energy for APV-PR interactions is compensated by a decrease in the polar solvation free energy such that the net binding affinity remains unchanged.
Abstract: However, the affinities of the drug resistant protease variants V32I, I50V, I54V, I54M, I84V and L90M to amprenavir are decreased 3 to 30-fold compared to the wild-type.
Interaction of I50V mutant and I50L/A71V double mutant HIV-protease with inhibitor TMC114 (darunavir): molecular dynamics simulation and binding free energy studies.
PMID: 22239286
2012
The journal of physical chemistry. B
Introduction: As for other approved PIs, several HIV-pr mutants were demonstrated to have drug resistance over the TMC114, like D30N and I50V, whereas L90M is well adapted by the TMC114.
Result: For example, L90M and V82F/I84V mutations open the flap a bit more in the mutant than the WT, whereas M46I mutation makes the flap more closed.
Emergence of an HIV-1 cluster harbouring the major protease L90M mutation among treatment-naive patients in Tel Aviv, Israel.
Abstract: CONCLUSION: There was an unexpectedly high rate of the major L90M PI resistance mutation in the MSM group.
Abstract: Phylogenetic analysis showed a tight cluster comprising 13 of 14 viruses harbouring the L90M major PI resistance mutation, suggesting a single infection source.
Drug resistance mutations in HIV pol sequences from Argentinean patients under antiretroviral treatment: subtype, gender, and age issues.
PMID: 21936717
2012
AIDS research and human retroviruses
Abstract: The most common DRMs were L10I, I54V, L90M, V82A, A71V, L10V, M46I, M184V, M41L, T215Y, D67N, L210W, K70R, N348I, V118I, K103N, Y181C, G190A, K101E, V108I, L100I, V90I, K101Q, and PMID: 22046345
2011
PloS one
Result: Both specimens harboured mutations F53L and L90M at PR and M41L, K103N, L210W and T215D at RT.
Emerging transmitted drug resistance in treatment-naive human immunodeficiency virus-1 CRF06_cpx-infected patients in Estonia.
PMID: 20964489
2011
Scandinavian journal of infectious diseases
Abstract: A total of 2.8% of sequences harboured mutations indicating nucleoside/nucleotide reverse transcriptase inhibitor resistance (M41L, M184V, M184I, T215C and T215D), 2.1% non-nucleoside reverse transcriptase inhibitor resistance (K103N, P225H) and 2.8% protease inhibitor resistance (M46I, L90M).
Gender differences in HIV drug resistance mutations and virological outcome.
PMID: 21190485
2011
Journal of women's health (2002)
Abstract: There were no major statistically significant differences in the baseline demographic, clinical, or genotypic characteristics between males and females before GRT except for race, presence of coexisting hepatitis B and C infection, prior diagnosis of tuberculosis, presence of thymidine analogue mutations (TAMs), and protease inhibitor (PI) mutations L90M and I84V (p < 0.05).
Differences in reversion of resistance mutations to wild-type under structured treatment interruption and related increase in replication capacity.
Introduction: The authors reported a faster rate of reversion for primary resistance mutations (K70R, M184I/V, T215Y/F in RT, and D30N, M46I/L, V82A, L90M in PR) compared to secondary mutations (M41L, D67N, T69D/N, L210W, K219Q/E in RT and L10I/V, L63P, A71V/T, V77I in PR)
HIV mutation literature information.
PMID: 
2012
Journal of acquired immune deficiency syndromes (1999)
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