HIV mutation literature information.


  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


  Extreme multidrug resistant HIV-1 protease with 20 mutations is resistant to novel protease inhibitors with P1'-pyrrolidinone or P2-tris-tetrahydrofuran.
 PMID: 23590295       2013       Journal of medicinal chemistry
Introduction: Recently, we characterized a clinically derived HIV-1 protease (PR20) bearing 20 mutations [Q7K, L10F, I13V, I15V, D30N, V32I, L33F, E35D, M36I, S37N, I47V, I54L, Q58E, I62V, L63P, A71V, I84V, N88D, L89T and L90M] and extremely resist


  Restriction fragment mass polymorphism (RFMP) analysis based on MALDI-TOF mass spectrometry for detecting antiretroviral resistance in HIV-1 infected patients.
 PMID: 23480551       2013       Clinical microbiology and infection
Abstract: The concordance rates between the RFMP and direct sequencing assays for the examined codons were 97% (K65R), 97% (T69Ins/D), 97% (L74VI), 97% (K103N), 96% (V106AM), 97% (Q151M), 97% (Y181C), 97% (M184VI) and 94% (T215YF) in the reverse transcriptase coding region, and 100% (D30N), 100% (M46I), 100% (G48V), 100% (I50V), 100% (I54LS), 99% (V82A), 99% (I84V) and 100% (L90M) in th


  "Description of the L76V resistance protease mutation in HIV-1 B and ""non-B"" subtypes."
 PMID: 23349869       2013       PloS one
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.
Result: Among subtype B samples, the major


  Cooperative effects of drug-resistance mutations in the flap region of HIV-1 protease.
 PMID: 23252515       2013       ACS chemical biology
Introduction: I54A has a PI susceptibility profile similar to I54V, unlike other substitutions such as I54L and I54M.


  Mutations selected in HIV-2-infected patients failing a regimen including atazanavir.
 PMID: 22977160       2013       The Journal of antimicrobial chemotherapy
Abstract: Besides I50L, four PR mutations previously associated with protease inhibitor resistance (I54L, I64V, V71I and I82F) and six PR mutations of unknown impact (V10I, E37D, S43T, K45R, I75V and F85L) in HIV-2 were also identified in this small group of patients.


  Virological response to darunavir in patients infected with HIV is linked to darunavir resistance-associated mutations corrected by the count of mutations with positive impact and is not associated with pharmacological and combined virological/pharmacological parameters.
 PMID: 21545648       2012       Fundamental & clinical pharmacology
Abstract: Darunavir GIQ is defined as the ratio between darunavir trough plasma concentration and the count of darunavir resistance-associated mutations (V11I, V32I, L33F, I47V, I50V, I54L/M, T74P, L76V, I84V, L89V) corrected or not corrected by the count of mutations with positive impact (V82A and E35D).


  Genotypic resistance profiles associated with virological failure to darunavir-containing regimens: a cross-sectional analysis.
 PMID: 22237471       2012       Infection
Abstract: At DRV failure, the major increase was still observed for V32I; I54L, V11I, T74P and I50V also increased.


  HIV-1 protease with 20 mutations exhibits extreme resistance to clinical inhibitors through coordinated structural rearrangements.
 PMID: 22404139       2012       Biochemistry
Result: However, the central yttrium has no direct or water-mediated interaction with flap residues, although a surface layer of water molecules is visible extending from the catalytic aspartate towards flap residue I54L.
Result: Six other mutations Q7K, L10F, L33F, I54L, N88D and L90M are located in the second shell with direct influence on the inhibitor-interacting residues.


  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



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