literature

HIV mutation literature information.

HIV-1 Gag mutations alone are sufficient to reduce darunavir susceptibility during virological failure to boosted PI therapy.

PMID: 32556165 2020 The Journal of antimicrobial chemotherapy

Table: L63P

Polymorphisms and drug resistance analysis of HIV-1 isolates from patients on first line antiretroviral therapy (ART) in South-eastern Nigeria.

PMID: 32267869 2020 PloS one

Result: Polymorphisms at known secondary mutation sites (K20I, M36I/L, H69K/R and L89M) were found in all the samples while L63T/P/S/Q was found in 83.3% (10/12) and 31.3% (5/16) of subtypes G/UG and CRF02_AG respectively.

Table: L63P

Table: L63T/P

Discussion: In addition, the mutations K14R, N37D/S/E/H and L63T/P/S/Q occurred in >= 25% of subtype G, UG and CRF02_AG patients, at a proportion that is significantly greater than in subtype B.

Discussion: Other mutations/polymorphisms that occurred at very high frequencies among patients in this study include;

PMID: 32264923 2020 BMC infectious diseases

Conclusion: A genotype resistance test (GRT) in June 2002 (Trugene HIV-1 Genotyping Assay, Siemens Healthcare Diagnostics GmbH, Eschborn, Germany) showed extensive resistance in the RT region (M41L, E44D, D67N, V118L, M184V, L210W, and T215Y) and the PR region (L10I, M46L, L63P, V82T, and L90M), and a tropism test in 2013 (envelope glycoprotein (gp)120 V3 loop sequencing) revealed a C-C chemokine receptor type 5 (CCR5) tropic virus with a false positive rate of 91.3% (geno2pheno c

Highly drug-resistant HIV-1 protease reveals decreased intra-subunit interactions due to clusters of mutations.

PMID: 31920003 2020 The FEBS journal

Result: L10I and L63P did not show structural changes in PRS5B but have been shown to help maintain thermal stability when combined with I84V.

HIV Viral Rebound Due to a Possible Drug-Drug Interaction between Elvitegravir/Cobicistat/Emtricitabine/Tenofovir Alafenamide and Calcium-Containing Products: Report of 2 Cases.

PMID: 30798679 2019 Journal of the International Association of Providers of AIDS Care

Conclusion: The genotype at this time demonstrated no reverse transcriptase (RT) gene mutations, but the following protease gene mutations: L10V, M36I, L63P, H69H/Y, A71T/A, and I93L.

Conclusion: The genotype performed at this time showed the following protease inhibitor gene mutations: I13I/V, E35D, D60E, L63P, I64V, and V77I and RT mutation V106I/V/M

Mechanism of Darunavir (DRV)'s High Genetic Barrier to HIV-1 Resistance: A Key V32I Substitution in Protease Rarely Occurs, but Once It Occurs, It Predisposes HIV-1 To Develop DRV Resistance.

PMID: 29511083 2018 mBio

Table: L63P

Discussion: In contrast, a set of data compiled for NDA21-976/S003 and NDA21-976/S004 clearly indicates that 10 amino acid substitutions including L10F, V32I, L33F, S37N, M46I, I47V, I50V, L63P, A71V, and I84V are the most prevalent (https://www.accessdata.fda.gov/drugsatfda_docs/label/2008/021976s003s004lbl.pdf).

Context-dependent autoprocessing of human immunodeficiency virus type 1 protease precursors.

PMID: 29338056 2018 PloS one

Result: Meanwhile, the F56C/L63P produced more p6*-PRb fragment than the WT (Fig 7E) but had much less p6*-PRc than the WT (Fig 7F).

Result: The F56C/L63P double mutation produced less mature PR than the WT control (Fig 7C).

Result: The wild type control (Fig 7A and 7B, the upper panels) was compared to a F56C/L63P double mutation in the proviral context.

A decade of viral mutations and associated drug resistance in a population of HIV-1+ Puerto Ricans: 2002-2011.

PMID: 28493944 2017 PloS one

Abstract: L63P and M184V were the dominant mutations observed for the protease (PRO) and reverse transcriptase (

Result: The 3 most prevalent HIV-1 resistance-associated mutations for PRO were L63P (73.9%), V77I (45.2%) and I13V (34.2%), whereas I50L, I50V and K20I were the least abundant mutations recorded during the 10-year period (Figs 2 and 4).

Discussion: Previous research shows that the most common PRO mutation observed in the Puerto Rican sample-L63P -which is estimated to occur in half of drug-naive patients, provides a strong adaptive benefit to HIV viruses replicating under drug pressure.

The HIV-1 late domain-2 S40A polymorphism in antiretroviral (or ART)-exposed individuals influences protease inhibitor susceptibility.

PMID: 27600154 2016 Retrovirology

Result: 4, when the baseline infectivity of F56C/L63P was matched to F56C and the parental virus (panel A), the double mutant exhibited IDV resistance similar to that observed for F56C alone (panel B) indicating that the L63P polymorphism made no detectable contribution.

Result: L63P is a common polymorphism, however, its frequency was found to increase in PR inhibitor-treated patients.

Result: For these studies, we combined the most radical of these substitutions, L63P, with the S40A/F56C mutation forming F56C/L63P.

Structural Studies of a Rationally Selected Multi-Drug Resistant HIV-1 Protease Reveal Synergistic Effect of Distal Mutations on Flap Dynamics.

PMID: 27992544 2016 PloS one

Result: This inactive protease with active site D25N mutation has 22 other mutations (L10I, V11I, L23I, V32I, L33F, S37N, M46I, I47V, I50V, F53L, I54V, Q58E, D60E, L63P, H69R, A71V, G73S, V77I, V82F, L89V, L90M, <

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