Prevalence and determinants of virological failure, genetic diversity and drug resistance among people living with HIV in a minority area in China: a population-based study.
Result: The most common mutations in NNRTIs were K103N/KN (64.69%), V179D/E (23.47%) and Y181C/YC/I (14.00%), they were M184V/MV/I (36.29%), T215F/FS/TNSY (7.50%) and K219Q (5.92%) in NRTIs, and they were Q58E/QE (4.93%), L10F/LFI (0.39%) and M46L (0.39%) in PIs.
Pretreatment resistance mutations and treatment outcomes in adults living with HIV-1: a cohort study in urban Malawi.
In vivo drug resistance mutation dynamics from the early to chronic stage of infection in antiretroviral-therapy-naive HIV-infected men who have sex with men.
Abstract: Four individuals exhibited additional DRMs (M46I/L; I47A; I54M, L100V) as HIV minority populations (abundance, 2-20%) that emerged during the chronic stage but ephemerally.
The genotype distribution, infection stage and drug resistance mutation profile of human immunodeficiency virus-1 among the infected blood donors from five Chinese blood centers, 2014-2017.
Abstract: 48 DRMs were identified from 43 samples, indicating a drug resistance prevalence of 12.1% (43/356), which include seven protease inhibitors (PIs) accessory DRMs (Q58E, L23I and I84M), two PIs major DRMs (M46I, M46L), seven nucleoside RT inhibitors DRMs (D67N, K70Q, K219R and M184L), and 32 non-nucleoside RT inhibitors DRMs (K103N, V179E, K238N, V179D, PMID: 30961560
2019
BMC infectious diseases
Result: PI resistance were detected in only two samples, being simultaneously resistant to ATV/r and LPV/r at a potential low level caused by M46I/L mutation.
Trends in the Molecular Epidemiology and Genetic Mechanisms of Transmitted Human Immunodeficiency Virus Type 1 Drug Resistance in a Large US Clinic Population.
Result: A Kaplan-Meier analysis could be performed for 18 TDRMs (K20T, L23I, K43T, M46I/L/V, I54V, M41L, L74I, M184V, L210W, K2
Discussion: In concordance with the three other studies on the persistence of TDRMs, for most PI mutations (I54V, K43T, L23I, M46I/L/V) a long mean survival time between 2.2 and 4.2 years was found in our study cohort, with the exception of K20T that had a mean survival time of one (95% CI 0.4-1.2) year.
Result: A shift of 0.8 A in M46L is observed in PRS17/CA-p2 in comparison to complex with DRV.
Result: Also, PR with individual mutations of M46L, G48V, and I54V in the flaps showed worse inhibition constants (Ki) for DRV and saquinavir relative to the wild-type PR.
Result: Flap mutations M46L, G48V, and I54V in PRS17 are implicated in the curling of flaps observed in the inhibitor-free structure.
Result: However, G48V together with M46L also alters the conformation of other flap residues
Characterisation of protease resistance mutations in a South African paediatric cohort with virological failure, 2011 - 2017.