Q148N, a Novel Integrase Inhibitor Resistance Mutation Associated with Low-Level Reduction in Elvitegravir Susceptibility.
PMID: 27009474
2016
AIDS research and human retroviruses
Introduction: A baseline genotypic resistance test revealed the nucleoside reverse transcriptase inhibitor-resistance mutations L210W and T215D that were interpreted as causing intermediate resistance to zidovudine and low-level resistance to tenofovir; the non-nucleoside reverse transcriptase inhibitor (NNRTI)-resistance mutations K101P and K103S that were interpreted as causing high-level resistance to each of the NNRTIs; and the protease inhibitor-resistance mutations D30N, L33F, I54V, N88D, and L90M
HIV Drug Resistance in Antiretroviral Treatment-Naive Individuals in the Largest Public Hospital in Nicaragua, 2011-2015.
Result: Most PI SDRMs were present only as low-abundance variants under the 5% threshold, including L23I, D30N, I47V, I50V, F53L, I54T, G73S, V82A, N83D, I84V, I85V, N88DS, and L90M (Fig 2).
Structural Studies of a Rationally Selected Multi-Drug Resistant HIV-1 Protease Reveal Synergistic Effect of Distal Mutations on Flap Dynamics.
Result: In PR20, four (D30N, V32I, I47V and I84V) of the 19 mutations alter residues in the active site cavity.
Binding of Clinical Inhibitors to a Model Precursor of a Rationally Selected Multidrug Resistant HIV-1 Protease Is Significantly Weaker Than That to the Released Mature Enzyme.
Result: Although major PI resistance mutations was not detected in the non-drug users, three major PI resistance mutations including L90M, M46I and D30N were detected in 4 (5.1 %) IDUs.
Result: In addition, D30N+M46I co-existed with G48E and K20I minor mutations, respectively, in 2 (4.2 %) ART-experienced IDUs.
Result: Interestingly, mutation L90M co-existed with K20R minor mutation in 1 (2.1 %) ART-experienced IDU, while D30N co-existed with T74S+K20R minor mutations in 1 (3.1 %) ART-naive IDU.
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Structural Basis of Why Nelfinavir-Resistant D30N Mutant of HIV-1 Protease Remains Susceptible to Saquinavir.
PMID: 25487655
2015
Chemical biology & drug design
Abstract: Although anti-HIV-1 protease drugs nelfinavir (NFV) and saquinavir (SQV) share common functional groups, D30N is a major resistance mutation against NFV but remains susceptible to SQV.
Abstract: Structural analysis showed that SQV forms two direct hydrogen bonds with the main chain atoms of the residues Asp29 and Asp30 that are not observed in the D30N-NFV complex.
Abstract: These could be the reasons why D30N is not a drug resistance mutation against SQV.
Abstract: We have determined the crystal structure of D30N mutant-tethered HIV-1 protease in complex with SQV to 1.79 A resolution.
Epidemiological Surveillance of HIV-1 Transmitted Drug Resistance in Spain in 2004-2012: Relevance of Transmission Clusters in the Propagation of Resistance Mutations.
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 to PIs (D30N, M46I/L, I54V/T, L76V, V82A, I84V, N88D
Drug-resistant HIV-1 protease regains functional dynamics through cleavage site coevolution.
Abstract: Yet with substrate coevolution, while the wild-type dynamic behavior is restored in both p1-p6 ((LP) (1'F)p1-p6D30N/N88D) and NC-p1 ((AP) (2) (V)NC-p1V82A) bound proteases, the dynamic behavior of the NC-p1 bound protease variants (NC-p1V82A and (AP) (2) (V)NC-p1V82A) rather resemble those of the proteases bound to the other substrates, which is consistent with experimental studies.
HIV mutation literature information.
PMID: 
2016
Journal of acquired immune deficiency syndromes (1999)
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