literature

HIV mutation literature information.

Elucidating a relationship between conformational sampling and drug resistance in HIV-1 protease.

PMID: 23566104 2013 Biochemistry

Introduction: D30N occurs specifically in response to nelfinavir treatment, whereas M36I and A71V, along with other non-active site substitutions, appear as a result of selective pressure of treatments using various protease inhibitors.

Introduction: In particular, SDSL-DEER was used to understand the effects of the accumulation of primary, D30N, and secondary mutations M36I and A71V on the flap conformational sampling of WT subtype B HIV-1 PR.

Method: Seven stabilized (Q7K, L33I, L63I) and inactive (D25N) constructs (Bsi) with engineered labeling sites (

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.

PMID: 23469241 2013 PloS one

Result: The latter differed significantly in the frequencies of the major resistance RT mutations T215FY and K219QE (NRTI) and of several secondary/accessory mutations, including: the protease mutations I13V, M36I, I62V, L63P, A71V, V77I, L89M and I93L (Table 6) and the RT mutations A98S, K101N, K103R and V179I

Table: A71V

Structural and thermodynamic basis of amprenavir/darunavir and atazanavir resistance in HIV-1 protease with mutations at residue 50.

PMID: 23365446 2013 Journal of virology

Abstract: Reduced affinity to both I50V/A71V and I50L/A71V double mutants is largely due to decreased binding entropy, which is compensated for by enhanced enthalpy for ATV binding to I50V variants and APV binding to I50L variants, leading to hypersusceptibility in these two cases.

Abstract: To explain how APV, DRV, and ATV susceptibility are influenced by mutations at residue 50 in HIV-1 protease, structural and binding thermodynamics studies were carried out on I50V/L-substituted protease variants in the compensatory mutation A71V background.

"Description of the L76V resistance protease mutation in HIV-1 B and ""non-B"" subtypes."

PMID: 23349869 2013 PloS one

5Result: Likewise, this cluster was confirmed also in HIV-1 ""non-B"" sequences, where the major PI RAM L76V, M46I, I54L and I84V grouped together with the secondary one A71V (bootstrap value = 0.86)."

Impact of lopinavir/ritonavir use on antiretroviral resistance in recent clinical practice.

PMID: 22733652 2012 The Journal of antimicrobial chemotherapy

Abstract: Mutations in the protease gene significantly selected between baseline and failure were L10V, K20R, L33F, M36I, I47V, I54V, A71V and I85V (P < 0.05).

Drug resistance mutations in HIV pol sequences from Argentinean patients under antiretroviral treatment: subtype, gender, and age issues.

PMID: 21936717 2012 AIDS research and human retroviruses

Abstract: The most common DRMs were L10I, I54V, L90M, V82A, A71V, L10V, M46I, M184V, M41L, T215Y, D67N, L210W, K70R, N348I, V118I, K103N, Y181C, G190A, K101E, V108I, L100I, V90I, K101Q, and

PMID: 22239286 2012 The journal of physical chemistry. B

Conclusion: As for the other protease inhibitors, the increase of the binding affinity implies that the double mutant I50L/A71V may be well adapted by the TMC114.

Conclusion: However, for the double mutant I50L/A71V, the increase in the binding affinity can be mainly attributed to the increase in electrostatic and van der Waals energies of residues Leu50 and Leu50' with considerable aid from the other flap residues Gly49', Ile47' and active site residue Ile84.

Conclusion: The double mutant I50L/A71V HIV-pr exhibits different conformation and dynamic behavior to the TMC114 inhibitor, e.g., closer movement of flaps, and flip-flop interaction between the catalytic Asp25 OD1/OD

Prevalence of Drug Resistance and Associated Mutations in a Population of HIV-1(+) Puerto Ricans: 2006-2010.

PMID: 22593823 2012 AIDS research and treatment

Result: Statistically significant differences between men and women were recorded for A71V (P = 0.05) and L90M (P = 0.04) in 2006, and M36I (P = 0.005) in 2008.

Prevalence of HIV Drug Resistance Mutations in HIV Type 1 Isolates in Antiretroviral Therapy Naive Population from Northern India.

PMID: 22496972 2012 AIDS research and treatment

Result: Accessory minor PI mutations K20R, M36I, and H69K were seen in 7.3% (5/68), 97% (66/68), and 49% (33/68) patients, respectively; L63P, A71E, A71V, I13V, L10V, K45I, and K45R were observed in one patient each.

Differences in reversion of resistance mutations to wild-type under structured treatment interruption and related increase in replication capacity.

PMID: 21297946 2011 PloS one

Introduction: The authors reported a faster rate of reversion for primary resistance mutations (K70R, M184I/V, T215Y/F in RT, and D30N, M46I/L, V82A, L90M in PR) compared to secondary mutations (M41L, D67N, T69D/N, L210W, K219Q/E in RT and L10I/V, L63P, A71V/T, V77I in PR)

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