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
Trends in the Molecular Epidemiology and Genetic Mechanisms of Transmitted Human Immunodeficiency Virus Type 1 Drug Resistance in a Large US Clinic Population.
Result: Of the 203 PI-associated SDRMs, the most common were L90M (33.5%), M46I/L (19.7%), I54V (10.8%), V82A/L/T (10.4%), and D30N plus N88D (9.8%).
Evolution of Protease Inhibitor Resistance in Human Immunodeficiency Virus Type 1 Infected Patients Failing Protease Inhibitor Monotherapy as Second-line Therapy in Low-income Countries: An Observational Analysis Within the EARNEST Randomized Trial.
Abstract: Common PI mutations were M46I, I54V, and V82A.
High predictive efficacy of integrase strand transfer inhibitors in perinatally HIV-1-infected African children in therapeutic failure of first- and second-line antiretroviral drug regimens recommended by the WHO.
PMID: 30891603
2019
The Journal of antimicrobial chemotherapy
Result: DRMs to PIs corresponded mainly to natural polymorphism in the P gene while only the major DRMs V82A/F (n = 3; 20%) and L33F (n = 1, 6.7%) could be found.
Result: Similar to V82S mutation in PRS17, V82A mutation is also expected to expand the binding site for P3 Arg, but other larger and beta-branched mutations may block the access to this site.
Result: Similar to V82S, V82A mutation opens up the S3 site for substrate recognition.
Result: The major conformation of P3 Arg in the PRV82A/CA-p2 complex forms van der Waals contact with Phe53 in the second strand of the flaps similar to the PR/CA-p2 complex, while the carbonyl of P4' Nle of the minor conformation related by 180 occupies the P3 Arg site observed in the PRS17/ PMID: 31266578
2019
South African medical journal
Abstract: The most frequent major PI mutations were V82A (76.2%), M46I/M46L (76.2%), I54V (62.0%) and L76V (33.3%).
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.
Table: V82A/L
Table: V82A
Genetic diversity and antiretroviral resistance-associated mutation profile of treated and naive HIV-1 infected patients from the Northwest and Southwest regions of Cameroon.
Result: Major protease inhibitor mutations were present in 3 (1.3%, 95% CI: 0.3-3.6%) of the sequences occurring as I54T-V82A, M46I and M46LV.
Result: The sequence with the non-polymorphic PI-selected mutations (I54T and V82A) confers HLR to nelfinavir and intermediate resistance to all other PI drugs except darunavir.
Survey of Pretreatment HIV Drug Resistance and Genetic Transmission Network Analysis Among HIV Patients in a High Drug-Use Area of Southwest China.
Result: In addition, 8 PI mutations were identified, of which the most common were I54V (1.5%) and V82A/I (1.5%), which can lead to resistance to darunavir (DRV), lopinavir (LPV) and atazanavir (ATV).
Analysis of HIV-1 diversity, primary drug resistance and transmission networks in Croatia.
Result: The sequence originating from the UK had a similar mutation pattern with additional SDRMs (PI: M46L, V82A and NRTI: T215Y).
Discussion: Phylogenetic inference indicated a transmission link with one UK sequence with a similar mutation pattern, PI: V32I, M46L, I47A, V82A + NRTI: T215Y + NNRTI: L100I, K103N.
HIV mutation literature information.
PMID: 
2019
PloS one
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