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
HIV-1 integrase polymorphisms are associated with prior antiretroviral drug exposure.
Introduction: However, in a small study conducted at Westmead Hospital, Sydney, Australia, G140S was detected in 2 INI-naive patients, as were the other accessory mutations: L74I/M (n = 8), T97A (n = 2), V151I (n = 3) and I203M (n = 4).
Introduction: In contrast, isolated L74A/I/M has no effect on in vitro resistance while G140S is associated with an in vitro 5-10 fold decrease in susceptibility (Personal communication with Merck Sharp & Dohme).
Profile of HIV type 1 infection and genotypic resistance mutations to antiretroviral drugs in treatment-naive HIV type 1-infected individuals in Hai Phong, Viet Nam.
PMID: 19239356
2009
AIDS research and human retroviruses
Abstract: We found RT inhibitor-associated major resistance mutations in 7/273 cases (2.6%; one occurrence each of L74I, M184I, and K219E; three cases of K103N; and two cases of G190E).
Natural polymorphisms of human immunodeficiency virus type 1 integrase and inherent susceptibilities to a panel of integrase inhibitors.
PMID: 19651917
2009
Antimicrobial agents and chemotherapy
Abstract: We identified polymorphisms V72I, L74I, T97A, V151I, M154I/L, E157Q, V165I, V201I, I203M, T206S, and S230N.
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.
Effects of HIV type-1 immune selection on susceptability to integrase inhibitor resistance.
Result: These seven sites were L74I/M at the C terminus of HLA-B*1510-restricted THLEGKIIL, 91 at p9 of YIEAEVIPA with unknown restriction, T97A at p2 of HLA-A*2601-restricted ETGQETAY, 126 at p9 of HLA-A*3002-restricted KIQNFRYY, 128 at p2 of HLA-A2-restricted AKAACWWAGI, 143 at p9 of HLA-B*1503-restricted KQEFGIPY and 165 at p2 of HLA-A*0205-restricted QVRDQAEHL.
Prevalence of M184V and K65R in proviral DNA from PBMCs in HIV-infected youths with lamivudine/emtricitabine exposure.
Abstract: K65R was associated with reduced susceptibility to tenofovir, didanosine, abacavir and lamivudine; L74V/I was associated with reduced susceptibility to abacavir and didanosine.
Abstract: HIV-1 with K65R or L74V/I alone were fully susceptible to zidovudine and stavudine.
Abstract: TAMs were rarely observed in combination with K65R, but frequently associated with L74V/I.
Abstract: The addition of M184V to either K65R or L74V/I improved susceptibility to tenofovir, zidovudine and stavudine, but reduced susceptibility to abacavir, didanosine and lamivudine.
Prevalence, genotypic associations and phenotypic characterization of K65R, L74V and other HIV-1 RT resistance mutations in a commercial database.
Abstract: A gradual accumulation of new mutations was observed in all patients, including G140S, Q148H and N155H in patient 1, L74I in patient 2, and G140S in patient 3.
HIV-1 subtype B protease and reverse transcriptase amino acid covariation.
Abstract: Different patterns of covariation were frequently observed for different mutations at the same position including the RT mutations T69D versus T69N, L74V versus L74I, V75I versus V75M, T215F versus T215Y, and K219Q/E versus K219N/R, and the protease mutations M46I versus M46L, I54V versus I54M/L, and N88D versus N88S.
HIV mutation literature information.
PMID: 
2009
AIDS (London, England)
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