Abstract: The non-nucleoside K103N+L100I mutations were observed at high frequency (15.5%) and were significantly associated with the nucleoside mutation L74V in BF recombinants.
Abstract: The results provide clinical evidence of a molecular interaction between K103N+L100I and L74V mutations at the reverse transcriptase gene in vivo, limiting the future use of second-generation non-nucleoside reverse transcriptase inhibitors such as etravirine.
Assessing subtype and drug-resistance-associated mutations among antiretroviral-treated HIV-infected patients.
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: Didanosine plays the principal role in the L74V emergence.
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 and
Comparative analysis of in vitro processivity of HIV-1 reverse transcriptases containing mutations 65R, 74V, 184V and 65R+74V.
Abstract: Virion-associated RTs of WT pNL4-3, K65R, L74V, M184V and 65R+74V were used to perform RT processivity assays in the presence of trap, poly(rC)-oligo(dG).
Introduction: Although each are clinically important, K65R and L74V rarely occur on the same virus genome (Winters et al., 1997), and Stanford HIV drug resistance database (web site: http://hivdb.stanford.edu) confirm this rarity.
Introduction: Among 23 patients who received 1-2 years of 2',3'-dideoxyinosine (ddI) therapy, only one showed the presence of K65R and L74V on the same genome.
Introduction: Analysis of clinical data on the risks and incidence of K65R and
Anti-human immunodeficiency virus activity, cross-resistance, cytotoxicity, and intracellular pharmacology of the 3'-azido-2',3'-dideoxypurine nucleosides.
PMID: 19596885
2009
Antimicrobial agents and chemotherapy
Abstract: Importantly, both 3'-azido-ddA and 3'-azido-ddG retain activity against viruses containing K65R, L74V, or M184V (IC50 change of <2.0-fold) and against those containing three or more thymidine analog mutations (IC50 change of <3.5-fold).
Structural basis for the role of the K65R mutation in HIV-1 reverse transcriptase polymerization, excision antagonism, and tenofovir resistance.
PMID: 19812032
2009
The Journal of biological chemistry
Abstract: These K65R-mediated effects on RT structure and function help us to visualize the complex interaction with other key nucleotide RT drug resistance mutations, such as M184V, L74V, and thymidine analog resistance mutations.
Introduction: Among the most frequent in treatment-experienced populations are M184V and TAMs, and less frequent but positively associated are M184V with K65R; in contrast, K65R and TAMs or K65R and L74V are rarely present together.
Discussion: 5) suggests that the constraint on Arg72 caused by the K65R mutation (via the
Five-year follow up of genotypic resistance patterns in HIV-1 subtype C infected patients in Botswana after failure of thymidine analogue-based regimens.
PMID: 19852859
2009
Journal of the International AIDS Society
Abstract: In contrast, L74V was more frequent among individuals from Group 2 (16.2% versus 7.7%).
Antiretroviral drug-resistant mutations at baseline and at time of failure of antiretroviral therapy in HIV type 1-coinfected TB patients.
PMID: 19895208
2009
AIDS research and human retroviruses
Abstract: Among NRTI mutations, M184V was the commonest followed by L74I/V.
Viremia, resuppression, and time to resistance in human immunodeficiency virus (HIV) subtype C during first-line antiretroviral therapy in South Africa.
HIV mutation literature information.
PMID: 
2010
Antiviral therapy
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