literature

Detection of Gag C-terminal mutations among HIV-1 non-B subtypes in a subset of Cameroonian patients.

PMID: 35082353 2022 Scientific reports

Introduction: Following the Stanford algorithm (mutation list), minor resistance mutations (L10F, V11I, K20TV, L23I, L33F, K43T, F53L, Q58E, A71IL, G73STCA, T74P, N83D, and L89V) are assumed to have ancillary roles such as compensation for lower efficiency of proteolysis caused by major mutations; major resistance mutations (V32I, M46IL, I47VA, G48VM,

PMID: 35061671 2022 PloS one

Table: N83D

Brief Report: Bictegravir/Emtricitabine/Tenofovir Alafenamide Efficacy in Participants With Preexisting Primary Integrase Inhibitor Resistance Through 48 Weeks of Phase 3 Clinical Trials.

PMID: 34897227 2022 Journal of acquired immune deficiency syndromes (1999)

Table: N83D

Diversity of HIV-1 Subtypes and Transmitted Drug-resistance Mutations Among Minority HIV-1 Variants in a Turkish Cohort.

PMID: 34802406 2022 Current HIV research

Abstract: M41L, L74I, K65R, M184V, and M184I related to NRTI, K103N to NNRTI, and N83D, M46I, I84V, V82A, L24I, L90M, I54V to the PI sites were identified using NGS.

HIV Drug Resistance Mutations Detection by Next-Generation Sequencing during Antiretroviral Therapy Interruption in China.

PMID: 33668946 2021 Pathogens (Basel, Switzerland)

Result: However, some minority DRMs at frequencies of 1%-5% disappeared, including N83D with PI-related, K70E, T215A, and K219E with NRTI-related and K101E, Y181C, H221Y and K238T with NNRTI-related, while others emerged, such as NNRTI-related V106A in patient GX088 at a frequency of 8.7%, and L23I, I47V and I84V with PI-related, D67N and

Phylogenetic and Drug-Resistance Analysis of HIV-1 Sequences From an Extensive Paediatric HIV-1 Outbreak in Larkana, Pakistan.

PMID: 34484134 2021 Frontiers in microbiology

Result: Similarly, DRM PI:N88D, associated with resistance against protease inhibitors (PI), such as atazanavir/ritonavir, and tipranavir/ritonavir was observed in two treatment-experienced participants, while DRMs PI:M46L, PI:D30N, PI:N83D, PI:K43T, PI:G73S, PI:L33F were seen in one treatment-experienced individual each (Table 3).

Table: N83D

Highly drug-resistant HIV-1 protease reveals decreased intra-subunit interactions due to clusters of mutations.

PMID: 31920003 2020 The FEBS journal

Result: By allowing a continuation of van der Waals contacts at the hinge-Loop 1 interface using a shorter side chain, M36I counterbalances the effects of E35N and N83D and stabilizing the hinge-loop.

Result: Comparison of the PRS5B/DRV hinge-region

Result: Comparison of the new PRS5B structures with equivalent PR, PRS17, and PR20 complexes illustrates how the additional mutation of N83D replaces direct hydrogen bonds with water-mediated interactions at the hinge-body interface.

Trend of HIV-1 drug resistance in China: A systematic review and meta-analysis of data accumulated over 17 years (2001-2017).

PMID: 31922125 2020 EClinicalMedicine

Table: N83D

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: N83D

Resistance profile of the HIV-1 maturation inhibitor GSK3532795 in vitro and in a clinical study.

PMID: 31622432 2019 PloS one

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