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 Nucleoside Reverse Transcriptase Inhibitors (NRTI), L100I, K101EP, K103NS, V106AM
Clinical, virological and biochemical evidence supporting the association of HIV-1 reverse transcriptase polymorphism R284K and thymidine analogue resistance mutations M41L, L210W and T215Y in patients failing tenofovir/emtricitabine therapy.
Result: Amino acid substitutions D67N, L74I, K223E and L228H associate with the TAM2 cluster, while V118I, V179I, M184V and R284K are linked to cluster (2) formed by mutations of the TAM1 pathway.
Table: L74I
HIV-1 integrase resistance among antiretroviral treatment naive and experienced patients from Northwestern Poland.
Result: Among virologically failing patients E157Q was noted in one patient with N155H mutant, in three E157Q variant was present at baseline and consistently in the sequences obtained on RAL therapy while in two patients either R263K or L74IL were present at baseline and disappeared in the subsequent sequences on virologically unsuccessful treatment.
Result: Other mutations and polymorphisms observed only in subtype B integrase sequences were L68V, T97A and V151I, while in non-B sequences R263K, E138D, L68IL and L74IL variant
Human Immunodeficiency Virus-1 Viral Load Is Elevated in Individuals With Reverse-Transcriptase Mutation M184V/I During Virological Failure of First-Line Antiretroviral Therapy and Is Associated With Compensatory Mutation L74I.
Abstract: Although attenuated in comparison to WT virus and single point mutants K65R, L74V and L74I; the double mutant K65R+L74I replicated efficiently in comparison to K65R+L74V mutant.
Abstract: Analysis of the HIV resistance database has revealed that similar to K65R+L74V, the double mutant K65R+L74I is also rare.
Abstract: CONCLUSIONS: The improved replication kinetics of K65R+L74I virus in comparison to K65R+L74V viruses was due to an increase in the processivity of
Resistance patterns selected by nevirapine vs. efavirenz in HIV-infected patients failing first-line antiretroviral treatment: a bayesian analysis.
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: 22180722
2011
Romanian biotechnological letters
Result: 19.5% of the patients presented L74V/I mutation that occur in patients with virologic failure while receiving non-TAM regimens and causes intermediate resistance to DDI and ABC, and a slight increase in susceptibility to AZT and TDF.
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: 20462946
2010
The Journal of antimicrobial chemotherapy
Method: We also examined the extent to which the 52 NNRTI-selected mutations covaried with mutations at 12 major nucleoside reverse transcriptase inhibitor (NRTI) resistance positions, including M41L, K65R, D67N, T69S_SS, K70E, K70R, L74V, L74I, V75M/T, Y115F, Q151M, M184V/I, L210W, T215F and T215Y.
Result: The strongest positive correlations were bet
Characterization of integrase region polymorphisms in HIV type 1 CRF06_cpx viruses in treatment-naive patients in Estonia.
PMID: 20849300
2010
AIDS research and human retroviruses
Abstract: No primary drug resistance mutations against integrase inhibitors were found, but resistance-associated polymorphisms such as V72I, L74I, V201I, and T206S were seen in more than 90% of viruses.
Human Immunodeficiency Virus-1 Viral Load Is Elevated in Individuals With Reverse-Transcriptase Mutation M184V/I During Virological Failure of First-Line Antiretroviral Therapy and Is Associated With Compensatory Mutation L74I.
Abstract: BACKGROUND: Very little is known about the alternative L74I mutation.
Abstract: CONCLUSIONS: This study shows that the L74I and the L74V correspond to two different mutation pathways, conferring probably different resistance and replication advantages on HIV depending on the context.
Abstract: METHODS: We focused on the treatment used at the exact time of any L74V or L74I emergences in 74 patients, and we compared the use of each nucleoside reverse transcriptase inhibitor (NRTI) separately and in combination between the 74I and the 74V groups.
Abstract: OBJECTIVE: To compare and clarify the role of each antiretroviral compound and the resistance background in the emergence of the L74I an