Discussion: We show here that D30N, N88D/S and L90 M also have high transmissibility and that other SDRMs have higher (M41L, T215Rev and K219E/N/Q/R for NRTIs and K101E/P for the NNRTIs) or lower transmissibility (K70E/R, L74I/V, and T215Y/F for NRTIs; Y181C/I/V for NNRTIs and I84 V and I54A/L/M/S/T/V for protease inhibit
A Comparative Insight into Amprenavir Resistance of Mutations V32I, G48V, I50V, I54V, and I84V in HIV-1 Protease Based on Thermodynamic Integration and MM-PBSA Methods.
PMID: 26317593
2015
Journal of chemical information and modeling
Abstract: Drug resistance of mutations V32I, G48V, I50V, I54V, and I84V in HIV-1 protease (PR) was found in clinical treatment of HIV patients with the drug amprenavir (APV).
Gag-Protease Sequence Evolution Following Protease Inhibitor Monotherapy Treatment Failure in HIV-1 Viruses Circulating in East Africa.
PMID: 26258548
2015
AIDS research and human retroviruses
Introduction: The major LPV resistance mutation I54V developed at failure in two patients (6 and 8) and V82A in two additional patients (4 and 15).
The use of dried blood spot specimens for HIV-1 drug resistance genotyping in young children initiating antiretroviral therapy.
PMID: 26192603
2015
Journal of virological methods
Introduction: Only one specimen was predicted to be resistant to protease inhibitors (PI) due to the presence of major and minor PI mutations (L10F, M46I, I54V, L76V and V82A) while 8 specimens had minor PI mutations (A71T (n=3), L10I/V (n=3) and M46L/T (n=2)).
Treatment-Emergent Mutations and Resistance in HIV-Infected Children Treated with Fosamprenavir-Containing Antiretroviral Regimens.
Result: At VF, the following major treatment-emergent PI mutations or mutation mixtures were detected: M46M/I, I50I/V, I54I/M/V, and I84I/V, and the virus developed FPV RS.
Effects of drug-resistant mutations on the dynamic properties of HIV-1 protease and inhibition by Amprenavir and Darunavir.
Abstract: Molecular dynamics simulations are performed to investigate the dynamic properties of wild-type HIV-1 protease and its two multi-drug-resistant variants (Flap + (L10I/G48V/I54V/V82A) and Act (V82T/I84V)) as well as
Discussion: The crystal structure comparison of flap variants (I50V, I54V, and I54M) bound with SQV and variants (G48V, I54V, and I54M) bound with DRV suggested that the change in polar interactions between protease and inhibitors have the best correlation with observed resistance mutations.
Epidemiological Surveillance of HIV-1 Transmitted Drug Resistance in Spain in 2004-2012: Relevance of Transmission Clusters in the Propagation of Resistance Mutations.
Result: Among the 44 sequences with TDR to PIs, the most common mutations were L90M (47.7%), M46L/I (33.3%), I54V/T (21.4%), and V82A (19%).
Result: It is noteworthy that several major mutations associated to high level resistance to NRTIs (K65R, L74V, Y115F, M184V and T215Y), to NNRTIs (l100I, K101E, K103N/S, V106M, Y181C, Y188L and G190A) and
Single Genome Analysis for the Detection of Linked Multiclass Drug Resistance Mutations in HIV-1-Infected Children After Failure of Protease Inhibitor-Based First-Line Therapy.
PMID: 25923117
2015
Journal of acquired immune deficiency syndromes (1999)
Abstract: In one child, the majority species contained M184V in reverse transcriptase linked to L10F, M46I/L, I54V, and V82A in PR and a triple-class drug-resistant variant with these mutations linked to the NNRTI mutation V108I.
Discussion: Age adjusted full-dose RTV can select M46I, I54V, and V82A in children, as well as L10F, M46L, and Q58E in adults.
Genetic Changes in HIV-1 Gag-Protease Associated with Protease Inhibitor-Based Therapy Failure in Pediatric Patients.
PMID: 25919760
2015
AIDS research and human retroviruses
Abstract: Major protease resistance mutations (M46I, I54V, and V82A) were identified in eight (40%) patients, as well as Gag cleavage site (CS) mutations (at codons 373, 374, 378, 428, 431, 449, 451, and 453) in nine (45%) patients.
The L33F darunavir resistance mutation acts as a molecular anchor reducing the flexibility of the HIV-1 protease 30s and 80s loops.
PMID: 29124158
2015
Biochemistry and biophysics reports
Method: MDR769 L33F is based on the previously studied multi-drug resistant variant 769, MDR769, which contains the mutations Q7K, L10I, M36V, M46L, I54V, I62V, L63P, A71V, V82T, I84V, L90M.
HIV mutation literature information.
PMID: 
2015
AIDS (London, England)
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