literature

Detection of Gag C-terminal mutations among HIV-1 non-B subtypes in a subset of Cameroonian patients.

PMID: 35082353 2022 Scientific reports

Introduction: Following the Stanford algorithm (mutation list), minor resistance mutations (L10F, V11I, K20TV, L23I, L33F, K43T, F53L, Q58E, A71IL, G73STCA, T74P, N83D, and L89V) are assumed to have ancillary roles such as compensation for lower efficiency of proteolysis caused by major mutations; major resistance mutations (V32I, M46IL, I47VA, G48VM,

PMID: 26695135 2015 BMC bioinformatics

Introduction: L23I, D30N, E35G, M46I/L/V, G48V, I54L, G73S/T/C/A, T74S, V82A/F/S/T, I84V, N88D/S and L90M are other mutations correlated to NFV resistance.

Low frequency of genotypic resistance in HIV-1-infected patients failing an atazanavir-containing regimen: a clinical cohort study.

PMID: 23711895 2013 The Journal of antimicrobial chemotherapy

Result: The remaining 43 minor atazanavir mutations were either not detected in this dataset (L10C, K20V, E34Q, F53Y, I54L/M/T/A, A71L, G73C/T, V82F and I93M) or were not significantly associated with atazanavir exposure (L10I/F/V, G16E, K20R/M/I/T, L24I, V32I, L33I/F/V, M36L/V, M46L, G48V, I54V

Trends in Genotypic HIV-1 Antiretroviral Resistance between 2006 and 2012 in South African Patients Receiving First- and Second-Line Antiretroviral Treatment Regimens.

PMID: 23840622 2013 PloS one

Method: The following non-polymorphic ARV-selected mutations were classified as drug resistance mutations (DRM): (i) the NRTI resistance mutations M41L, A62V, K65RN, D67NG, T69D, T69 insertions, T69 deletion, K70REGQ, L74VI, V75MT, F77L, Y115F, F116Y, Q151M, M184VI, L210W, T215YFSDCIV, and K219QENR; (ii) the

Population-based monitoring of emerging HIV-1 drug resistance on antiretroviral therapy and associated factors in a sentinel site in Cameroon: low levels of resistance but poor programmatic performance.

PMID: 23991142 2013 PloS one

Abstract: RESULTS: At baseline, a prevalence of 3.6% (5/139) HIVDR was observed [protease inhibit

Result: Sequences from 5 patients were identified with drug resistance-associated mutations, giving a prevalence of 3.6% (5/139) HIVDR, among which 3 resistance mutations to protease inhibitors (M46I, G73A, L90LM); 2 to nucleoside reverse transcriptase inhibitors (M184V), T215F); and 3 to non-nucleoside reverse transcriptase inhibitors (K103N, Y181C, Y181YC, M230ML).

Table: G73A

Low prevalence of transmitted drug resistance in patients newly diagnosed with HIV-1 infection in Sweden 2003-2010.

PMID: 22448246 2012 PloS one

Method: The following resistance mutations were scored: to nucleoside reverse transcriptase inhibitors (NRTIs): M41L, K65R, D67N/G/E, T69D/insertion, K70R/E, L74V/I, V75M/T/A/S, F77L, Y115F, F116Y, Q151M, M184V/I, L210W, T215Y/F/I/S/C/D/V/E, K219Q/EN/R; to non-nucleoside revers

Drug resistance mutations in patients infected with HIV-2 living in Spain.

PMID: 21558334 2011 The Journal of antimicrobial chemotherapy

Abstract: No major mutations associated with drug resistance in HIV-1 were recognized in 29 PR, 20 RT and 5 INT sequences from antiretroviral-naive HIV-2 individuals, although natural polymorphisms with potential effects on susceptibility to PR inhibitors were recognized at 10 positions (L10V/I, V32I, M36I, M46I, I47V, Q58E, A71V/I, G73A, V82I and L89I/V) and for nucleoside reverse transcriptase inhibitors at three positions (T69N, V75I

Distinct resistance mutation and polymorphism acquisition in HIV-1 protease of subtypes B and F1 from children and adult patients under virological failure.

PMID: 18992847 2009 Infection, genetics and evolution

Method: Mutations L10F/I/R/V, K20M/R, L24I, L33F, M36I, F53L, I54V/L/A/M/T/S, L63P, A71V/T, G73C/S/T/A, V77I and N88D/S were considered as minor resistance mutations and were also analyzed separately and together as a group.

Discussion: The mutations L10F/R, K20I, V32I, I47V/A, I50L/V,

PMID: 19143530 2009 Clinical infectious diseases

Result: Naturally occurring HIV-2 PR polymorphisms that are associated with PI resistance in HIV-1 were common; major (V32I/L, M46I/V, and I47V) and minor (L10V/I, E35G/R, Q58E, A71V/I, and G73A/T) PI resistance mutations were found in all 23 patients.

A novel substrate-based HIV-1 protease inhibitor drug resistance mechanism.

PMID: 17227139 2007 PLoS medicine

Method: In addition, the model was also adjusted on use of nelfinavir at baseline and on the number of PI mutations (L10IRVF, K20RM, M36I, A71VT, G73SA, V82AFTS, L90M) found to be associated with the virological response in univariate analyses in this subset of patients.