The L76V mutation in HIV-1 protease is potentially associated with hypersusceptibility to protease inhibitors Atazanavir and Saquinavir: is there a clinical advantage?
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.
Drug resistance mutations in patients infected with HIV-2 living in Spain.
PMID: 21558334
2011
The Journal of antimicrobial chemotherapy
Abstract: No major mutations associated with drug resistance in HIV-1 were recognized in 29 PR, 20 RT and 5 INT sequences from antiretroviral-naive HIV-2 individuals, although natural polymorphisms with potential effects on susceptibility to PR inhibitors were recognized at 10 positions (L10V/I, V32I, M36I, M46I, I47V, Q58E, A71V/I, G73A, V82I and L89I/V) and for nucleoside reverse transcriptase inhibitors at three positions (T69N, V75I
Resolution of discordant HIV-1 protease resistance rankings using molecular dynamics simulations.
PMID: 21902276
2011
Journal of chemical information and modeling
Abstract: Mutations at only three positions ( L10I , A71IV, andL90M ) influenced the resistance level assigned to the sequence.
Can linear regression modeling help clinicians in the interpretation of genotypic resistance data? An application to derive a lopinavir-score.
Abstract: Of note, the P225H and A71V are 'minor' drug-resistance mutations conferring only minimal drug-resistance phenotypes in the absence of major mutations.
Abstract: The prevalence of protease inhibitor mutations was 45%, with major mutation L90M seen in 33% and minor mutation A71V in 36% of samples.
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 L10F/I/R/V, K20M/R, L24I, L33F, M36I, F53L, I54V/L/A/M/T/S, L63P, A71V/T, G73C/S/T/A, V77I and N88D/S were considered as minor resistance mutations and were also analyzed separately and together as a group.
Discussion: Interestingly, did not observe a higher prevalence of D30N, but rather a higher prevalence of A71V and V77I in subtype B compared with subtype F viruses isolated from treated pat
Emergence of multiclass drug-resistance in HIV-2 in antiretroviral-treated individuals in Senegal: implications for HIV-2 treatment in resouce-limited West Africa.
Result: Naturally occurring HIV-2 PR polymorphisms that are associated with PI resistance in HIV-1 were common; major (V32I/L, M46I/V, and I47V) and minor (L10V/I, E35G/R, Q58E, A71V/I, and G73A/T) PI resistance mutations were found in all 23 patients.
Analysis and characterization of dimerization inhibition of a multi-drug-resistant human immunodeficiency virus type 1 protease using a novel size-exclusion chromatographic approach.
Result: PRMDR contains multiple drug-resistant mutations (L10I, K45R, I54V, L63P, A71V, V82T, L90M and I93L) and is highly resistant to a number of active-site inhibitors, although it remains sensitive to the experimental active-site inhibitor JE-2147.
HIV mutation literature information.
PMID: 
2011
AIDS research and therapy
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