HIV mutation literature information.


  HIV multi-drug resistance at first-line antiretroviral failure and subsequent virological response in Asia.
 PMID: 25141905       2014       Journal of the International AIDS Society
Result: Major PI RAMs found in the two patients were M46L, G48V, V82A, N83D and L90M.


  Transmitted HIV drug resistance in treatment-naive Romanian patients.
 PMID: 23592112       2013       Journal of medical virology
Result: Both isolates presented the M46L mutation-conferring intermediate-level resistance to nelfinavir and potential low-level resistance to lopinavir and atazanavir-alone in the subtype C strain and along with multiple other resistance mutations, such as L24I, I47V, F53L, I54V, and V82A in the F1 strain.


  Restriction fragment mass polymorphism (RFMP) analysis based on MALDI-TOF mass spectrometry for detecting antiretroviral resistance in HIV-1 infected patients.
 PMID: 23480551       2013       Clinical microbiology and infection
Abstract: The concordance rates between the RFMP and direct sequencing assays for the examined codons were 97% (K65R), 97% (T69Ins/D), 97% (L74VI), 97% (K103N), 96% (V106AM), 97% (Q151M), 97% (Y181C), 97% (M184VI) and 94% (T215YF) in the reverse transcriptase coding region, and 100% (D30N), 100% (M46I), 100% (G48V), 100% (I50V), 100% (I54LS), 99% (V82A), 99% (I84V) and 100% (L90M) in th


  Heat shock protein 90AB1 and hyperthermia rescue infectivity of HIV with defective cores.
 PMID: 23200770       2013       Virology
Method: The I54V and V82A PR-mutant HIV clone has been described earlier.
Method: The transduced Jurkat E6-1 cells were inoculated at a MOI of 0.05 with WT HIV and CA-mutant HIV, and the PR-mutant HIV PRI54V+V82A served as a positive control for rescue of reduced infectivity of the mutant viruses.
Result: In parallel, we included the PR-mutant PRI54V+V82A HIV as a positive control to validate the rescue by overexpression of HSP90AB1.


  Significantly improved HIV inhibitor efficacy prediction employing proteochemometric models generated from antivirogram data.
 PMID: 23436985       2013       PLoS computational biology
Figure: M46L, A71T, V82A, V82S) but also several novel mutations (e.g.


  Novel P2 tris-tetrahydrofuran group in antiviral compound 1 (GRL-0519) fills the S2 binding pocket of selected mutants of HIV-1 protease.
 PMID: 23298236       2013       Journal of medicinal chemistry
Introduction: In order to study the molecular basis for the potency of inhibitor 1 against drug resistant viral strains, crystal structures of inhibitor 1 complexes with PR mutants bearing single substitutions of R8Q, D30N, I50V, I54M and V82A (PRR8Q, PRD30N, PRI50V, PRI54M and PRV82A) were analyzed.
Introduction: The mutation V82A in the active site cavity can eliminate interactions with inhibitor, and also exhibits a shift of its main chain atoms to adapt to inhibitor.
Method: Mutants (R8Q, D30N,


  Antiviral resistance and correlates of virologic failure in the first cohort of HIV-infected children gaining access to structured antiretroviral therapy in Lima, Peru: a cross-sectional analysis.
 PMID: 23280237       2013       BMC infectious diseases
Method: The OLA was conducted according to the NIH protocol for mutations at HIV-1B protease positions D30N, I50V, V82A, V82S, V82T, I84V, N88D, and L90M as well as reverse transcriptase positions K103N, Y181C, K65R, T215F, T215Y, M184V, and Q151M.


  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


  "Description of the L76V resistance protease mutation in HIV-1 B and ""non-B"" subtypes."
 PMID: 23349869       2013       PloS one
5Result: Significant differences in the prevalence of PI RAMs detected with the L76V between subtype B and ""non-B"" samples were found at 4 positions with a higher prevalence of the V32I, M46I/L, V82A/F/L/T/S and L90M mutations in subtype B than in ""non-B"" samples: 10 vs 0%, P = 0.04; 92 vs 82%, P = 0.036; 52 vs 26%, P = 0.0011; and 42 vs 18%, P = 0.002, respectively."
5Result: Then, the most prevalent mutation found with L76V was the V82A/F/L/T/S (52%) in subtype B samples and I84V (36%) in ""non-B"" samples."
Result: This cluster was linked to L24I, I54V, and


  Cooperative effects of drug-resistance mutations in the flap region of HIV-1 protease.
 PMID: 23252515       2013       ACS chemical biology
Introduction: Besides G48V or I54V, Flap+(I54V) has an additional active site mutation V82A, as does Flap+(I54A).
Introduction: Both G48V and V82A are associated with SQV resistance.
Introduction: Flap+(I54V) is a drug resistant protease variant containing a combination of active site and flap mutations (L10I/G48V/I54V/V82A) (Figure 1) that often occur together in treated patients.



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