Abstract: Two had SDRMs to nucleoside reverse-transcriptase inhibitors (D67G and L210W), three had SDRMs to nonnucleoside reverse transcriptase inhibitors (G190A, G190S, and K101E), and one had SDRMs to protease inhibitors (N88D).
Within-host co-evolution of Gag P453L and protease D30N/N88D demonstrates virological advantage in a highly protease inhibitor-exposed HIV-1 case.
Abstract: Among these, we focused on associations between Gag-P453L, the P5' position of the p1/p6 cleavage-site mutation, and PR-D30N/N88D nelfinavir-resistant mutations, and attempted to clarify their virological significance in vitro by constructing recombinant clones.
Abstract: Furthermore, database analysis indicated that the P453L(Gag)/D30N(PR)/N88D(PR) association was not specific only to our clinical case, but was common among AIDS patients.
Abstract: The results showed that P453L(
Prevalence of drug resistance and associated mutations in a population of Hiv-1+ Puerto Ricans in 2005.
PMID: 23875516
2010
Boletin de la Asociacion Medica de Puerto Rico
Result: For women, N88D was among the top ten mutations (11.7%) while in males its expression was 9.3%.
In Vivo validation of a bioinformatics based tool to identify reduced replication capacity in HIV-1.
PMID: 21603285
2010
The open medical informatics journal
Discussion: N88D/S did not have a significant effect on fitness in the statistical model and was not tested.
Discussion: HIV variants with both the D30N and N88D mutation was also found to have decreased replication capacity in vitro, including subtype C strains.
Discussion: Similarly, patients with the D30N mutation often develop the N88D/S mutation.
The effect of clade-specific sequence polymorphisms on HIV-1 protease activity and inhibitor resistance pathways.
Abstract: AE protease has been observed to develop resistance through a nonactive-site N88S mutation in response to nelfinavir (NFV) therapy, whereas clade B protease develops both the active-site mutation D30N and the nonactive-site mutation N88D.
Abstract: The D30N/N88D mutations in clade B resulted in a significant loss of affinity for NFV and, to a lesser extent, for DRV.
Understanding the HIV-1 protease nelfinavir resistance mutation D30N in subtypes B and C through molecular dynamics simulations.
PMID: 20541446
2010
Journal of molecular graphics & modelling
Abstract: The compensatory mutations N83T and N88D, observed in vitro and in vivo when subtype C acquires D30N, were also studied.
HIV drug resistance surveillance using pooled pyrosequencing.
Distinct resistance mutation and polymorphism acquisition in HIV-1 protease of subtypes B and F1 from children and adult patients under virological failure.
PMID: 18992847
2009
Infection, genetics and evolution
Method: Mutations L10F/I/R/V, K20M/R, L24I, L33F, M36I, F53L, I54V/L/A/M/T/S, L63P, A71V/T, G73C/S/T/A, V77I and N88D/S were considered as minor resistance mutations and were also analyzed separately and together as a group.
Result: Conversely, mutations L10V, K20M, L33F, M36I, G73S, and N88D were significant
Within-host co-evolution of Gag P453L and protease D30N/N88D demonstrates virological advantage in a highly protease inhibitor-exposed HIV-1 case.
PMID: 19720046
2009
Biochemical and biophysical research communications
Abstract: N88D and N88S are two such mutations which occur in the non-active site region of the enzyme.
Abstract: We have determined crystal structures of unliganded N88D and N88S mutants of HIV-1 protease to resolution of 1.65A and 1.8A, respectively.
Abstract: While structural effects of N88D are very subtle, the mutation N88S has caused a significant conformational change in D30, an active site residue crucial for substrate and inhibitor binding.
Role of atazanavir in the treatment of HIV infection.
PMID: 19436623
2009
Therapeutics and clinical risk management
Introduction: Mutations more significant to be included in the GIQ model are the following: L10F/I/V, K20M/R, L24I, D30N, V32I, L33F, M36I/L, I47V/A, G48V, I50V, I50L, F53L, I54V/L/A/M/T/S, L63P, A71V/T, G73S, V77I, V82A/F/T, I84V, N88D/S and
HIV mutation literature information.
PMID: 
2011
AIDS (London, England)
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