literature

HIV mutation literature information.

Structural studies of antiviral inhibitor with HIV-1 protease bearing drug resistant substitutions of V32I, I47V and V82I.

PMID: 31092330 2019 Biochemical and biophysical research communications

Method: The clone for triple mutant PRTri (V32I, I47V and V82I) includes optimizing mutations of Q7K, L33I, and L63I to decrease autoproteolysis, and C67A, C95A to eliminate cysteine-thiol oxidation.

Drug Resistance Mutation L76V Alters Nonpolar Interactions at the Flap-Core Interface of HIV-1 Protease.

PMID: 30288468 2018 ACS omega

Method: PRWT and PRL76V proteins contain optimizing mutations Q7K/L33I/L63I to reduce autoproteolysis and C67A/C95A to prevent thiol bond formation.

HIV-1 infection among crack cocaine users in a region far from the epicenter of the HIV epidemic in Brazil: Prevalence and molecular characteristics.

PMID: 30016324 2018 PloS one

Abstract: Five isolates had secondary mutations to protease inhibitors (K20M, L10V, L33I, A71T, A71V).

Result: No major mutation to PI was identified; however, five isolates presented minor PI mutations (K20M: BRGO_CK4, subtype B; A71V: BRGO_CK600, subtype B; L10V: BRGO_CK496, subtype B; A71T and L33I: BRGO_CK311, subtype B; L10V: BRGO_CK117, subtype C).

Exploration of the effect of sequence variations located inside the binding pocket of HIV-1 and HIV-2 proteases.

PMID: 29636521 2018 Scientific reports

Result: Five of these mutations (Q7K, L33I, L63I, C67A, and C95A) correspond to classical experimental mutations introduced to minimize autoproteolysis and to prevent cysteine-thiol oxidation of PR1.

Room Temperature Neutron Crystallography of Drug Resistant HIV-1 Protease Uncovers Limitations of X-ray Structural Analysis at 100 K.

PMID: 28195728 2017 Journal of medicinal chemistry

Method: The PRTM has substitutions V32I, I47V and V82I associated with drug resistance, which are in addition to five stabilizing substitutions Q7K, L33I, L63I, C67A and C95A.

Effect of internal cleavage site mutations in human immunodeficiency virus type 1 capsid protein on its structure and function.

PMID: 27516963 2016 FEBS open bio

Method: The construction of HIV-1 PR coding region containing five stabilizing mutations (Q7K, L33I, L63I, C67A, and C95A) was described previously 44, 45.

Prevalence of Transmitted Drug Resistance Mutations in HIV-1-Infected Drug-Naive Patients from Urban and Suburban Regions of Kenya.

PMID: 26401720 2016 AIDS research and human retroviruses

Abstract: Among these mutations, L33I was the most prevalent mutation.

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

PMID: 26870021 2016 Frontiers in microbiology

Table: L33I

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

Figure: Mutations introduced in WT PR to restrict autoproteolysis (Q7K, L33I and L63I) and avoid cysteine-thiol oxidation (C67A and C95A) are indicted by asterisks.

From antiretroviral therapy access to provision of third line regimens: evidence of HIV Drug resistance mutations to first and second line regimens among Ugandan adults.

PMID: 28010730 2016 BMC research notes

Abstract: Seven of the 36 patients on second line ART had major Protease Inhibitor (PI) associated DRMS including; V82A-7.0%, I54V, M46I and L33I (all 5.0%).

Result: The most common major PI-resistance mutations associated with the highest levels of phenotypic resistance were: V82A:7.0% and I54V, M46I, L33I (all 5.0%).

Table: L33I

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