The L76V drug resistance mutation decreases the dimer stability and rate of autoprocessing of HIV-1 protease by reducing internal hydrophobic contacts.
Result: For example, Tm values for ATV resistant mutant I50L/A71V and multi-drug resistant mutant V82F/I84V were both higher than the values observed for PR by 2.2 and 4 C, respectively.
HIV-1 protease mutations and protease inhibitor cross-resistance.
PMID: 20660676
2010
Antimicrobial agents and chemotherapy
Abstract: Of the mutations with the greatest effect on PI susceptibility, I84AV was associated with decreased susceptibility to eight PIs; V32I, G48V, I54ALMSTV, V82F, and L90M were associated with decreased susceptibility to six to seven PIs; I47A, G48M, I50V, L76V, V82ST, and N88S were associated with decreased susceptibility to four to five PIs; and D30N, PMID: 20516562
2010
Antiviral therapy
Abstract: By contrast, addition of APV to I50L-containing recombinant viruses was not associated with reversion.
Abstract: METHODS: Recombinant viruses containing in vitro and in vivo selected I50L and I50V proteases were constructed and cultured in increasing concentrations of APV or ATV, respectively.
Abstract: Phenotypically, both sequential and concomitant ATV-APV pressure yielded viruses resistant to all the drugs tested, although the emergence of I50L by ATV pressure on APV-resistant variants was associated with a reduced resistance to APV and darunavir.
Abstract: RESULTS: ATV or APV alone selected I50L- or I50V-containing variants.
Abstract: Subsequent addition of ATV to I50V-conta
Human immunodeficiency virus type 1 protease-correlated cleavage site mutations enhance inhibitor resistance.
Abstract: Several patterns were frequently observed, including mutations in the NC-p1 cleavage site in combination with I50L, V82A, and I84V within the protease and mutations within the p1-p6 cleavage site in combination with D30N, I50V, and I84V within the protease.
Distinct resistance mutation and polymorphism acquisition in HIV-1 protease of subtypes B and F1 from children and adult patients under virological failure.
PMID: 18992847
2009
Infection, genetics and evolution
Method: Mutations D30N (NFV), V32I (LPV), M46I/L (IDV/RTV), I47V/A (LPV/RTV), G48V (SQV), I50L/V (APV), V82A/F/T/S (LPV/IDV/RTV), I84V (APV/IDV/RTV) and L90M (SQV/NFV) were considered as major resistance mutations and were analyzed separately for each PI as well as quantitatively all together.
Discussion: The mutations L10F/R, K20I, V32I, I47V/A, I50L/V, I54L/A/M/T/S, PMID: 19436623
2009
Therapeutics and clinical risk management
Abstract: A signature mutation at the protease gene, I50L, may confer loss of susceptibility to the drug.
Introduction: In PI-naive patients, the most frequent mutation at failure under ATV is I50L, while in PI-experienced patients mutations I84V and N88S are more commonly selected.
Introduction: In this situation, the resistance barrier may be confined to a single key mutation (eg, I50L).
Introduction: Mutations more significant to be included in the GIQ model are the following: L10F/I/V, K20M/R, L24I, D30N, V32I
Interaction of I50V mutant and I50L/A71V double mutant HIV-protease with inhibitor TMC114 (darunavir): molecular dynamics simulation and binding free energy studies.
Abstract: I50 L caused resistance to atazanavir in all 31 mutation contexts, but was associated with higher susceptibility for other PIs.
Abstract: I50 L-associated shifts in FC were evaluated using drug-specific CCOs.
Abstract: BACKGROUND: The HIV-1 protease mutation I50 L causes atazanavir resistance but increases susceptibility to other PIs.
Abstract: CONCLUSIONS: The PI mutation I50 L causes clinically relevant resistance and increased susceptibility to atazanavir and other PIs respectively.
Abstract: OBJECTIVE: To evaluate I50 L's effect on susceptibility to 8 PIs, in a large geno
Evolution of the HIV-1 protease region in heavily pretreated HIV-1 infected patients receiving Atazanavir.
Atazanavir: simplicity and convenience in different scenarios.
PMID: 17376023
2007
Expert opinion on pharmacotherapy
Abstract: Naive patients receiving ATV boosted with ritonavir do not develop PI mutations at failure, whereas unboosted ATV in the same scenario induces the I50L mutation, which does not confer cross-resistance to other PIs.
HIV mutation literature information.
PMID: 
2011
Biochemistry
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