Functional correlation between a novel amino acid insertion at codon 19 in the protease of human immunodeficiency virus type 1 and polymorphism in the p1/p6 Gag cleavage site in drug resistance and replication fitness.
Abstract: Population-based sequence analysis revealed the presence of a variant of human immunodeficiency virus type 1 (HIV-1) containing an insertion of amino acid Ile in the protease gene at codon 19 (19I) and amino acid substitutions in the protease at codons 21 (E21D) and 22 (A22V) along with multiple mutations associated with drug resistance, M46I/P63L/A71V/I84V/I93L, in a patient who had failed protease inhibitor (PI) therapy.
Abstract: To characterize the role of these mutations in drug susceptibility and replication capacity, a chimeric HIV-1 strain containing the 19I/E21D
High HIV type 1 subtype diversity and few drug resistance mutations among seropositive people detected during the 2005 second generation HIV surveillance in Madagascar.
PMID: 16796535
2006
AIDS research and human retroviruses
Abstract: According to the ANRS September 2005 DRM list and algorithm, no DRM was detected in the reverse transcriptase and only one strain bore three major DRM in the protease M46I, I84V, and L90M leading to resistance to indinavir, saquinavir, nelfinavir, atazanavir/ritonavir, and possibly lopinavir.
Temporal characterization of drug resistance associated mutations in HIV-1 protease and reverse transcriptase in patients failing antiretroviral therapy.
Abstract: From 1999 to 2003, resistance-mutations to drugs with high genetic-barrier significantly decreased (L90M/V82A/M46I/I54V/G73S/I84V/G48V for PIs; M41L/D67N/L210W/V1181 for NRTIs, p < 0.05), while mutations to drugs with low genetic-barrier increased (D30N in protease, M184V/K103N/V108I in reverse transcriptase, p < 0.05).
Emergence of antiretroviral therapy resistance-associated primary mutations among drug-naive HIV-1-infected individuals in rural western Cameroon.
PMID: 16885781
2006
Journal of acquired immune deficiency syndromes (1999)
Abstract: Protease inhibitor-associated primary resistance mutations were found in 4 (7.4%) cases: M46L with full clones in 1 case, and M46I, M46L, and V82A as minor populations in 1 case each.
Quantitative SNP-detection method for estimating HIV-1 replicative fitness: application to protease inhibitor-resistant viruses.
Abstract: HIV-1 can survive under indinavir pressure by acquiring M46I mutation, as with acquisition of the L90M mutation under saquinavir pressure.
Abstract: Using this new competitive growth assay, replicative fitness of drug-resistant HIV-1 containing an M46I amino acid mutation in the protease was assessed in the presence or absence of indinavir.
[Background study of HIV-1 drug resistant mutations in treatment-naive patients in liaoning province].
PMID: 17121220
2006
Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae
Abstract: RESULTS: Totally 91 sequences were obtained, 3 of which displayed M46I mutations in the protease gene.
Natural polymorphisms of HIV type 2 pol sequences from drug-naive individuals.
PMID: 17147507
2006
AIDS research and human retroviruses
Abstract: In particular, the M46I substitution in the protease was detected in 90% of the sequences analyzed, which, together with the other substitutions identified, may indicate a reduced susceptibility of HIV-2-infected drug-naive patients to PI.
N88D facilitates the co-occurrence of D30N and L90M and the development of multidrug resistance in HIV type 1 protease following nelfinavir treatment failure.
PMID: 17209774
2006
AIDS research and human retroviruses
Abstract: In 16 patients having isolates with more than one combination of mutations at positions 30, 88, and 90, all exhibited one of the steps in the following progression: D30N-->D30N+N88D-->D30N+N88D+L90M-->D30N+N88D+L90M+(L33F+/-I84V or M46I/L+/-I54V).
Compensatory mutations at the HIV cleavage sites p7/p1 and p1/p6-gag in therapy-naive and therapy-experienced patients.
Abstract: The analysis of CS and PR mutations in therapy-experienced viruses revealed several positive correlations--A431V with L24I-M46I/L-I54V-V82A; I437V with I54V-V82F/T/S; L449V with I54M/L/S/T/A; and L449F/R452S/P453L: with D30N-I84V--whereas P453L and V82A were negatively correlated.
Performance of drug-resistance genotypic assays among HIV-1 infected patients with predominantly CRF02_AG strains of HIV-1 in Abidjan, Cote d'Ivoire.
HIV mutation literature information.
PMID: 
2006
Journal of virology
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