Result: Four mutations T69D (NRTI), K103N/S (NNRTI), M46I/L (PI) and L90M (PI) showed significantly different percentages in different subtypes (p < 0.05) (Table 1).
Table: L90M
Highly drug-resistant HIV-1 protease reveals decreased intra-subunit interactions due to clusters of mutations.
Result: Another study on single mutants V32I, L33F, L76V, and L90M showed how remote mutations can impact inhibitor binding by altering protein ensemble dynamics through a rearranged network of residues circulating to the active site.
Pretreatment HIV drug resistance spread within transmission clusters in Mexico City.
PMID: 31819984
2020
The Journal of antimicrobial chemotherapy
Result: The most frequent PI mutations included M46I/L and L90M.
Resistance profile of the HIV-1 maturation inhibitor GSK3532795 in vitro and in a clinical study.
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
Molecular Genetics and the Incidence of Transmitted Drug Resistance Among Pre-Treatment HIV-1 Infected Patients in the Eastern Cape, South Africa.
Abstract: Four major protease inhibitor (PI) related mutations (I54V, V82A/L, L76V and L90M) were observed in seven patients while several other minor and accessory PIs were also identified.
Surveillance of transmitted HIV drug resistance among newly diagnosed, treatment-naive individuals at a county HIV clinic in Santa Clara County.
Result: The prevalence of individual PI TDRMs was generally <0.5% except for L90M (1.0%).
Discussion: The low prevalence of PI TDR and the predominance of L90M among PI TDRMs is consistent with other US-based studies.
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 Result: PI-R substitutions were observed in 10% (55/543), with M46I/L (4.1%, 22/543) and L90M (2.4%, 13/543) most frequently detected.
Molecular Determinants of Epistasis in HIV-1 Protease: Elucidating the Interdependence of L89V and L90M Mutations in Resistance.
1Abstract: The focus of our investigation is a patient-derived isolate, with 24 mutations that we call ""KY""; this variant includes the L89V and L90M mutations."
Abstract: In this study, we investigated the interdependence between the L89V and L90M mutations and their effects on DRV binding.
Abstract: Molecular dynamics simulations of these DRV-bound protease variants reveal how the L90M mutation induces structural changes throughout the enzyme that undermine the binding interactions.
Abstract: When a leucine to valine mutation at residue 89 is present simultaneously with the L90M mutation, a rescue of catalytic efficiency is observed.
Introduction: As DRV binds wild-type (WT) sequences of HI
Prevalence and persistence of transmitted drug resistance mutations in the German HIV-1 Seroconverter Study Cohort.
Result: For a number of TDRMs, no loss could be observed during the observation period (S1 Table) and, according to their maximal duration of observation, the following TDRMs seem to survive for lengthy periods in the absence of ART: the NRTI resistance mutations D67N (5.9 years), K70R (6.9 years), F77L (10.2 years), T215E (5.9 years) and K219Q (5.9 years), the NNRTI resistance mutations A98G (6.5 years) and Y188L (5.9 years) as well as the PI mutations I54L (5.9 years) and L90M (8.4 years) (S1 Table).
Discussion: We could not obtain a Kaplan-Meier estimate for
ViMRT
HIV mutation literature information.
PMID: 
2020
The Journal of infectious diseases
