Simultaneous detection of major drug resistance mutations in the protease and reverse transcriptase genes for HIV-1 subtype C by use of a multiplex allele-specific assay.
PMID: 23985909
2013
Journal of clinical microbiology
Abstract: All the wild-type and mutant alleles were unequivocally distinguished with plasmid templates, and the limits of detection were 1.56% for K219Q and K219E, 3.13% for L76V, 6.25% for K65R, K70R, L74V, L100I, K103N, K103R, Q151M, Y181C, and I47V, and 12.5% for M41L, K101P, K101E, V106A, V106M, Y115F, M184V, PMID: 23904291
2013
The Journal of infectious diseases
Table: I47A
Trends in Genotypic HIV-1 Antiretroviral Resistance between 2006 and 2012 in South African Patients Receiving First- and Second-Line Antiretroviral Treatment Regimens.
Method: The following protease mutations were considered LPV/r-resistance mutations: L10F, L24I, V32I, L33F, M46IL, I47A, I50V, I54MLV, L76V, V82ATSFMC, I84V, L89V, L90M.
Method: The following non-polymorphic ARV-selected mutations were classified as drug resistance mutations (DRM): (i) the NRTI resistance mutations M41L, Table: I47A
Transmission patterns of HIV-subtypes A/AE versus B: inferring risk-behavior trends and treatment-efficacy limitations from viral genotypic data obtained prior to and during antiretroviral therapy.
Method: In our study, samples with at least one of the major PI RAM of the IAS-USA list as follows: D30N, V32I, M46I/L, I47A/V, G48V, I50L/V, I54L/M, Q58E, T74P, L76V, V82A/F/L/T/S, N83D, I84V, N88S, L90M were considered as PI-resistant issued from PI-experienced patients.
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
Can linear regression modeling help clinicians in the interpretation of genotypic resistance data? An application to derive a lopinavir-score.
Discussion: In the Stanford IS this mutation is currently given a weight of +25 which is the 2nd highest weight, after that given to I47A (weight = +50) while the Rega IS assign a weight of 0.6, remarkably similar to ours but about half the weight given to I54V (Table S1).
Influence of major HIV-1 protease inhibitor resistance mutations on CTL recognition.
PMID: 21107269
2011
Journal of acquired immune deficiency syndromes (1999)
Abstract: CONCLUSIONS: PI mutations, G48V, M46I, and I47A, can abrogate CTL recognition, indicating potential interactions between development of drug resistance and CTL response.
Abstract: Furthermore, M46I, I47A, and I50V could impair or abolish CTL recognition in many patients.
Abstract: Recently, we identified KMIGGIGGF (KF9) as a HLA-B*1501-restricted CTL epitope, including several major PI resistance mutations (M46I/L, I47A/V, G48V, I50V).
HIV-1 protease codon 36 polymorphisms and differential development of resistance to nelfinavir, lopinavir, and atazanavir in different HIV-1 subtypes.
PMID: 20404123
2010
Antimicrobial agents and chemotherapy
Abstract: The presence of I47A in LPV-selected I36 CRF02_AG virus conferred higher-level resistance than L76V in LPV-selected M36 CRF02_AG virus.
HIV-1 protease mutations and protease inhibitor cross-resistance.
PMID: 20660676
2010
Antimicrobial agents and chemotherapy
Abstract: Of the mutations with the greatest effect on PI susceptibility, I84AV was associated with decreased susceptibility to eight PIs; V32I, G48V, I54ALMSTV, V82F, and L90M were associated with decreased susceptibility to six to seven PIs; I47A, G48M, I50V, L76V, V82ST, and N88S were associated with decreased susceptibility to four to five PIs; and D30N,
ViMRT
HIV mutation literature information.
PMID: 
2013
Journal of clinical microbiology
