literature

HIV mutation literature information.

Treatment Outcomes and Resistance Patterns of Children and Adolescents on Second-Line Antiretroviral Therapy in Asia.

PMID: 27355415 2016 Journal of acquired immune deficiency syndromes (1999)

Result: Data on PI resistance mutations were available among 50 (68%) children, and included any major LPV mutation (L76V, V82A, V82S; 8%), >=6 LPV mutations (2%), any major darunavir (DRV) mutation (I84V, L76V; 2%), and any major ATV mutation (I84V, N88S; 4%) (Table 2).

Binding of Clinical Inhibitors to a Model Precursor of a Rationally Selected Multidrug Resistant HIV-1 Protease Is Significantly Weaker Than That to the Released Mature Enzyme.

PMID: 27039930 2016 Biochemistry

Abstract: Three of five mutations in PR(S17) correlating with major drug resistance, M46L, G48V, and V82S, and five of 11 natural variations differ from the mutations in two clinically derived extreme mutants, PR20 and PR22 bearing 19 and 22 mutations, respectively.

Result: Mutations in PRS17 associated with resistance to multiple drugs are M46L, G48V, I54V, V82S and L90M.

Result: Unlike mutations V82S, proximal to the active site pocket, and G48V and I54V in the flap

Unique Flap Conformation in an HIV-1 Protease with High-Level Darunavir Resistance.

PMID: 26870021 2016 Frontiers in microbiology

Table: V82S

HIV-1 Drug Resistance Mutations: Potential Applications for Point-of-Care Genotypic Resistance Testing.

PMID: 26717411 2015 PloS one

Result: The remaining 8% of viruses with predicted intermediate or high-level LPV resistance had a combination of two or more PI DRMs with lower mutation scores, including V32I, M46I, I54M/L/V, I47V, V82S/T/M and L90M.

Table: V82S

Structural studies on molecular mechanisms of Nelfinavir resistance caused by non-active site mutation V77I in HIV-1 protease.

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.

Introduction: The other mutations which were co-occurring with DBM and TPM included major mutations like- M46IL, I54MV, I84V, L90M, N88S, V32I,

PMID: 26558396 2015 PloS one

Table: V82S

Significantly improved HIV inhibitor efficacy prediction employing proteochemometric models generated from antivirogram data.

PMID: 23436985 2013 PLoS computational biology

Result: For the PIs mutations that are accurately reproduced include D30N, I50L, V82S, and I84, while the I64L and I93M mutations are assigned less importance than in previous work.

Figure: M46L, A71T, V82A, V82S) but also several novel mutations (e.g.

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

Table: V82A/S

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 protease mutations were considered LPV/r-resistance mutations: L10F, L24I, V32I, L33F, M46IL, I47A, I50V, I54MLV, L76V, V82ATSFMC, I84V, L89V, L90M.

Table: V82T/S

Persistence of HIV-1 transmitted drug resistance mutations.

PMID: 23904291 2013 The Journal of infectious diseases

Table: V82S

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