Abstract: RESULTS: We cloned a set of GFP-PR reporters, some of which possess a simple, well-defined drug-resistant PR mutant (G48V L90M, V82A, A71V V82T I84V, D30N, K45I); another four complex PR mutants were obtained from patients undergoing HAART.
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: Longitudinal analysis revealed that the P63L/A71V/I93L changes were present prior to PI therapy.
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
Virological responses to atazanavir-ritonavir-based regimens: resistance-substitutions score and pharmacokinetic parameters (Reyaphar study).
Abstract: The Reyaphar score included 12 baseline protease substitutions from the International AIDS Society USA list that were associated with poorer VR: L10I/F/R/V, K20I/M/R, L241, M461/L, 154L/M/T/V, L63P, A71I/L/V/T, G73A/C/F/T, V771, V82A/F/S/T, 184V, L90M and the polymorphism substitution Q58E.
A Comparative Molecular Dynamics, MM-PBSA and Thermodynamic Integration Study of Saquinavir Complexes with Wild-Type HIV-1 PR and L10I, G48V, L63P, A71V, G73S, V82A and I84V Single Mutants.
PMID: 16970402
2006
Journal of medicinal chemistry
Abstract: Comparison of eight structures exploring the binding of four similar inhibitors--SE, SQ (S-hydroxyethylamine isostere), OE (ethyleneamine), and QF34 (hydroxyethylene)--to wild-type and A71V/V82T/I84V HIV-1 protease elucidates the principles of altered interaction with changing conditions.
Abstract: The A71V mutation, which is distant from the active site, causes changes in the structure of the enzyme detectable by the means of X-ray structure analysis, and a route of propagation of the effect toward the active site is proposed.
Abstract: Two new X-ray structures of an HIV-1 protease mutant (A71V, V82T, I84V) in complex with inhibitors SE and SQ, pseudotetrapeptide i
[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: Minor resistance mutation rate to protease inhibitors was 100%, including types of L63P (60.4%), V77I (60.4%), M36I/V (31.9%), A71V/T (22.0%), L10I (8.8%), and K20R (6.6%).
[Study of resistance using the TRUGENE HIV-1 genotyping system and analysis of agreement between rule-based algorithms and virtual phenotyping].
PMID: 15757587
2005
Enfermedades infecciosas y microbiologia clinica
Abstract: For the IP: key mutations L90M (26.1%), M46I (18.1%) and V82AFTS (12.9%); and accessory mutations L63P (50.5%), A71V (27.2%), L10I (25.2%) and M36I (19.2%).
Human immunodeficiency virus type 1 (HIV-1) genotyping in Rio de Janeiro, Brazil: assessing subtype and drug-resistance associated mutations in HIV-1 infected individuals failing highly active antiretroviral therapy.
PMID: 15867968
2005
Memorias do Instituto Oswaldo Cruz
Abstract: The K103N mutation was the most prevalent to the non-nucleoside RT inhibitor and the resistance associated to protease inhibitor showed the minor mutations L63P, L10F/R, and A71V as the more prevalent.
[Primary resistance to antiretroviral therapy in patients with HIV/AIDS in Chile].
Abstract: Ten mutations were identified: V179D, L10I/V, M361, L63P, A71T/V, Y115F, V118I and K20R.
[Genotypic antiretroviral resistance testing and phylogenetic analysis of protease and reverse transcriptase in antiretroviral drug-naive AIDS patients in Henan province].
PMID: 16053762
2005
Zhonghua liu xing bing xue za zhi
Abstract: Minor mutation rate of resistance was 100%, including types of L63PS (36/36), I93L (35/36), V77IL (34/36), A71IVT (10/36) and D60E (2/36).
Selection and characterization of HIV-1 showing reduced susceptibility to the non-peptidic protease inhibitor tipranavir.
Abstract: At the end of the selection experiments, viruses harbouring 10 mutations in the protease (L10F, I13V, V32I, L33F, M36I, K45I, I54V, A71V, V82L, I84V) as well as a mutation in the CA/SP1 gag cleavage site were selected and showed 87-fold decreased susceptibility to tipranavir.
HIV mutation literature information.
PMID: 
2006
Journal of clinical virology
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