HIV mutation literature information.


  Resistance profile of the HIV-1 maturation inhibitor GSK3532795 in vitro and in a clinical study.
 PMID: 31622432       2019       PloS one
Method: Participants with a history of genotypic/phenotypic drug resistance to protease inhibitors (PIs) or with HIV-1 genotypic drug resistance to PIs at baseline (including D30N, M46I/L, I47V/A, G48V, I50L, I54M/L, Q58E, T74P, L76V, V82A/F/L/T/S, N83D, I84V, N88S, or L90M) were excluded, despite any reported effects of PI resistance or resistance


  Switching to bictegravir/emtricitabine/tenofovir alafenamide maintained HIV-1 RNA suppression in participants with archived antiretroviral resistance including M184V/I.
 PMID: 31430369       2019       The Journal of antimicrobial chemotherapy
Method: Primary PI-R substitutions were D30N, V32I, M46I/L, I47V/A, G48V, I50V/L, I54M/L, Q58E, T74P, L76V, V82A/F/L/S/T, N83D, I84V, N88S and L90M in PR.


  Highly Drug-Resistant HIV-1 Protease Mutant PRS17 Shows Enhanced Binding to Substrate Analogues.
 PMID: 31172041       2019       ACS omega
Abstract: The loss of beta-branched side chain by V82S mutation initiates a shift in 80's loop and reshapes the S3/S3' subsite, which enhances substrate binding with new hydrogen bonds and van der Waals interactions that are absent in the wild-type structures.
Result: Altered Recognition of CA-p2 P3 Arg Modulated by V82S Mutation.
Result: In both PRS17-P41/p2-NC and PRS17-P61/p2-NC complexes, the P3' Arg binds in the same pocket albeit the guanidine head of P3' Arg is tilted toward V82S mutation due to the lack of a beta-branched Cdelta atom in residue 82.


  [Genetic analysis of the mutations in HIV-1 infected population in Ecuador].
 PMID: 29652972       2018       Revista chilena de infectologia
Abstract: Results The most frequent mutations were M184V/I, K101E/P/H, K103N/S, D30N, M46L/I, I54L/M, V82T/F/A/S/L and L90M in adults and F77L, K103N/S, M46L/I, V82T/F/A/S/L and L90M in children.


  Virological response, HIV-1 drug resistance mutations and genetic diversity among patients on first-line antiretroviral therapy in N'Djamena, Chad: findings from a cross-sectional study.
 PMID: 29126456       2017       BMC research notes
Abstract: Overall, 32% (37/116) patients presented >= one major drug resistant mutation(s), with 29% (34/116) to nucleos(t)ide reverse transcriptase inhibitors (67% [29/43] M184V/I, 30% [13/43] T215Y/F, 19% [8/43] V75A/F/I/L/M, 9% [4/43] K70P/R/W, 9% [4/43] K219E/N/Q and 5% [2/43] A62V); 86% (37/43) to non-nulceos(t)ide reverse transcriptase inhibitors (30% [13/43] K103N/S/E, 26% [11/43] Y181C/V/F/L, 2% [1/43] L100I, 2% [1/43] F227L, 2% [1/43] P225H); and 2% (1/43


  Temporal Patterns and Drug Resistance in CSF Viral Escape Among ART-Experienced HIV-1 Infected Adults.
 PMID: 28328546       2017       Journal of acquired immune deficiency syndromes (1999)
Result: The most common PI mutations were V82A/T/F/S/I; V32I mutation was present in 3 cases, and has been associated with high level of resistance in combination with other PI mutations.


  Week 48 resistance analysis of Elvitegravir/Cobicistat/Emtricitabine/Tenofovir DF versus Atazanavir + Ritonavir + Emtricitabine/Tenofovir DF in HIV-1 infected women (WAVES study GS-US-236-0128).
 PMID: 28891788       2017       HIV clinical trials
Method: Primary PI-R substitutions assessed were D30N, V32I, L33F, M46I/L, I47A/V, G48V, I50L/V, I54L/M, Q58E, T74P, L76V, V82A/F/L/S/T, I84V, N88S, and L90M in PR.


  Treatment Outcomes and Resistance Patterns of Children and Adolescents on Second-Line Antiretroviral Therapy in Asia.
 PMID: 27355415       2016       Journal of acquired immune deficiency syndromes (1999)
Result: Data on PI resistance mutations were available among 50 (68%) children, and included any major LPV mutation (L76V, V82A, V82S; 8%), >=6 LPV mutations (2%), any major darunavir (DRV) mutation (I84V, L76V; 2%), and any major ATV mutation (I84V, N88S; 4%) (Table 2).


  Binding of Clinical Inhibitors to a Model Precursor of a Rationally Selected Multidrug Resistant HIV-1 Protease Is Significantly Weaker Than That to the Released Mature Enzyme.
 PMID: 27039930       2016       Biochemistry
Abstract: Three of five mutations in PR(S17) correlating with major drug resistance, M46L, G48V, and V82S, and five of 11 natural variations differ from the mutations in two clinically derived extreme mutants, PR20 and PR22 bearing 19 and 22 mutations, respectively.
Result: Mutations in PRS17 associated with resistance to multiple drugs are M46L, G48V, I54V, V82S and L90M.
Result: Unlike mutations V82S, proximal to the active site pocket, and G48V and I54V in the flap


  Unique Flap Conformation in an HIV-1 Protease with High-Level Darunavir Resistance.
 PMID: 26870021       2016       Frontiers in microbiology
Table: V82S



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