Abstract: M89I/V should be considered a secondary PI mutation with an important effect on nelfinavir susceptibility in the presence of L90M.
Abstract: However, when combined with L90M, a significantly reduced susceptibility to nelfinavir was observed (P < 0.05) in comparison with strains with L90M alone.
Detection of minor populations of drug-resistant HIV-1 in acute seroconverters.
Abstract: Minor populations of drug-resistant variants were detected by quantitative real-time polymerase chain reaction using allele-discriminating oligonucleotides for three key resistance mutations: L90M (protease), K103N and M184V (reverse transcriptase).
Abstract: The L90M mutation was found in one of 49 (2%), the K103N mutation in five of 49 (10.2%) and the M184V mutation in six of 49 (12.2%) patients, respectively.
Structured treatment interruptions in primary HIV-1 infection: the ANRS 100 PRIMSTOP trial.
PMID: 16249705
2005
Journal of acquired immune deficiency syndromes (1999)
Abstract: A major protease inhibitor resistance mutation (L90M) developed in 3 patients.
HIV-1 genotypes related to failure of nelfinavir as the first protease inhibitor treatment.
PMID: 16270125
2005
The Brazilian journal of infectious diseases
Abstract: Failure with nelfinavir has been associated with two protease gene mutations, D30N and L90M.
Abstract: In the tests for protease gene mutations, the D30N mutation was found in 57%, L90M in 18% and the wild-type virus in 25%.
Wide-open 1.3 A structure of a multidrug-resistant HIV-1 protease as a drug target.
Abstract: A second structural change is triggered by the L90M mutation that results in reshaping the 23-32 segment.
Substitutions in the reverse transcriptase and protease genes of HIV-1 subtype B in untreated individuals and patients treated with antiretroviral drugs.
Abstract: In PR, a L90M (T-->A substitution) was prevalent in 47% of protease inhibitor (PI)-treated patients.
Resistant mechanism against nelfinavir of human immunodeficiency virus type 1 proteases.
PMID: 16851048
2005
The journal of physical chemistry. B
Abstract: L90M mutation
Abstract: Among patients who failed in the inhibitor nelfinavir (NFV) treatment, D30N, N88D, and L90M mutations of HIV-1 protease are often observed.
Abstract: Despite the serious clinical problem, it is not clear how these mutations, especially nonactive site mutations N88D and L90M, affect the affinity of NFV or why they cause the resistance to NFV.
Abstract: In this study, we executed molecular dynamics simulations of the NFV-bound proteases in the wild-type and D30N, N88D, D30N/N88D, and L90M mutants.
Substitutions in the Reverse Transcriptase and Protease Genes of HIV-1 Subtype B in Untreated Individuals and Patients Treated With Antiretroviral Drugs.
PMID: 19825125
2005
Journal of the International AIDS Society
Abstract: In PR, a L90M (T-->A substitution) was prevalent in 47% of protease inhibitor (PI)-treated patients.
Result: Among major resistance mutations, 47% of PI-treated patients harbored the L90M mutation, which results from a T A transversion.
Table: L90M
Incidence of resistance in a double-blind study comparing lopinavir/ritonavir plus stavudine and lamivudine to nelfinavir plus stavudine and lamivudine.
PMID: 14702153
2004
The Journal of infectious diseases
Abstract: Primary mutations related to nelfinavir resistance (D30N and/or L90M) were observed in 43 (45%) of 96 nelfinavir-treated subjects.
Effect of polymorphisms on the replicative capacity of protease inhibitor-resistant HIV-1 variants under drug pressure.
PMID: 14759236
2004
Clinical microbiology and infection
Abstract: Using HIV-1 variants resistant to the protease inhibitors saquinavir (G48V/L90M) or indinavir (A71V/V82T/I84V), viral replication was studied in the presence or absence of inhibitor and a mutation at position 63.
HIV mutation literature information.
PMID: 
2005
AIDS (London, England)
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