Result: Also, one Croatian patient with a complex pattern of resistance (SDRM to PI: I84V + NRTI: M184MIV, T215S, L210W + NNRTI: K101E, Y181C, G190A, P225PH) was observed in a transmission pair with a Serbian sequence with a similar SDRM pattern with one additional SDRM (PI: M46I), indicating cross border transmission of multi-class drug 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: The next most common SDRMs, V32I, I50V/L, L76V, and I84V, each occurred in <=5 individuals.
An in silico pharmacological approach toward the discovery of potent inhibitors to combat drug resistance HIV-1 protease variants.
PMID: 30506751
2019
Journal of cellular biochemistry
Abstract: Herein, we strive for compounds that can stifle the function of wild-type (WT) HIV-1 PR along with four major single mutants (I54M, V82T, I84V, and L90M) instigating resistance to the PIs using in silico approach.
Structural Adaptation of Darunavir Analogues against Primary Mutations in HIV-1 Protease.
Abstract: Considerable losses of potency were observed against protease variants with I84V and I50V mutations for all three inhibitors.
Result
Result: Against I84V and I50V mutations, which are located directly at the pocket where P1' moiety binds, UMass1 experienced a similar reduction in potency as DRV [Table 1].
Result: Against I84V mutation, enhanced packing at the P1' moiety of UMass6 resulted in overall better interactions and potency.
Result: All three protease variants had a single mutation that altered the shape of the hydrophobic S1/S1' pocket of HIV-1 protease: I50V, V82I and I84V.
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: I84V
Molecular Determinants of Epistasis in HIV-1 Protease: Elucidating the Interdependence of L89V and L90M Mutations in Resistance.
Introduction: Primary drug resistant mutations, such as I50V and I84V, occur proximal to the active site and impact inhibitor binding by altering the direct interactions between the protease and inhibitor.
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
Emergence of HIV-1 drug resistance mutations in mothers on treatment with a history of prophylaxis in Ghana.
Result: The major DRAMs to PIs seen in the group was I84V; the minor drug resistance mutations seen were A71V, L89 V and M46MV.
Discussion: Mutation I84V emerged in the Protease gene associated with resistance to the PIs recommended for use in Ghana, ie NFV and Ritonavir boosted Lopinavir (LPV/r).
Mechanism of Darunavir (DRV)'s High Genetic Barrier to HIV-1 Resistance: A Key V32I Substitution in Protease Rarely Occurs, but Once It Occurs, It Predisposes HIV-1 To Develop DRV Resistance.
Introduction: The most DRV-resistant isolate, HIV-1DRVRP51, had acquired four major amino acid substitutions in its protease (V32I, L33F, I54M, and I84V), which have been shown to be responsible for the DRV resistance of HIV-1DRVRP51.
Table: I84V
Figure: (A and B) rHIVWT, rHIVV32I/I54M, rHIVL33F/I84V, and rHIVV32I/L33F/I54M/I84V (A) and rHIVV32I, rHIVL33F, rHIVI54M, and rHIVI84V (B) were propagated in the presence of increasing concentrations of DRV in MT-4 cells.
Figure: In the selection with DRV, proviral DNA was extracted at week 50 for HIVWT and HIVL33F, at week 36 for HIVV32I, at weeks 7, 24, a
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).
HIV mutation literature information.
PMID: 
2019
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