Transmission patterns of HIV-subtypes A/AE versus B: inferring risk-behavior trends and treatment-efficacy limitations from viral genotypic data obtained prior to and during antiretroviral therapy.
Sequence variability in p6 gag protein and gag/pol coevolution in human immunodeficiency type 1 subtype F genomes.
PMID: 23458243
2013
AIDS research and human retroviruses
Abstract: Also, in our dataset of subtype F genomes a strong association between mutation P5L in the p1/p6 cleavage region of gag and the nelfinavir (NFV) resistance mutation N88D(PR) was found with no impact on the preference for any of the NFV resistance pathways.
Novel P2 tris-tetrahydrofuran group in antiviral compound 1 (GRL-0519) fills the S2 binding pocket of selected mutants of HIV-1 protease.
PMID: 23298236
2013
Journal of medicinal chemistry
Result: Similar changes in interactions of residues 30 and 88 have been reported in mutants containing D30N and N88D and also proposed to effect inhibition.
Discussion: Considering the positive association of mutation D30N and N88D, it would be interesting to study how N88D influences the structure of D30N in complex with this new inhibitor 1.
Persistence of HIV-1 transmitted drug resistance mutations.
PMID: 23904291
2013
The Journal of infectious diseases
Table: N88D
HIV-1 Protease and Substrate Coevolution Validates the Substrate Envelope As the Substrate Recognition Pattern.
PMID: 24348205
2012
Journal of chemical theory and computation
Conclusion: In this study, structural properties of two drug resistant PR variants (V82A and D30N/N88D) and the substrates that coevolved with these two variants (AP2VNC-p1 and LP1'Fp1-p6/SP3'Np1-p6, respectively) were investigated in conformational ensembles obtained from MD simulations.
Result: For example, the PR: substrate vdW interaction potential of WTp1-p6D30N/N88D is 1.9 +- 0.2 kcal/mol (Figure 1H) less favorable than that of WTp1-p6WT.
Result: Similarly, in the presence of D30N/N88D mutations in the PR, LP1'F and SP3'N sub
HIV-1 protease with 20 mutations exhibits extreme resistance to clinical inhibitors through coordinated structural rearrangements.
Result: D30N is the only mutation of a charged first shell residue in PR20 and second shell mutation N88D may compensate for the altered charge.
Result: Analysis of mutation patterns in eight thousand and sixty virus isolates reveals that N88D is positively associated with D30N, and facilitates the occurrence of major resistance mutations D30N and L90M resulting in multidrug resistance.
Result: Furthermore, PR20 possesses a network of internal mutations (L10F, I13V, I15V, L33F, M36I, N88D and
PMID: 22401672
2012
Journal of medicinal chemistry
Abstract: Crystal structures at resolutions of 1.25-1.55 A were analyzed for complexes of 1 with the PR containing major drug resistant mutations, PR(I47V), PR(L76V), PR(V82A), and PR(N88D).
Abstract: Mutations of I47V and V82A alter residues in the inhibitor-binding site, while L76V and N88D are distal mutations having no direct contact with the inhibitor.
Abstract: Substitution of a smaller amino acid in PR(I47V) and PR(
The impact of the nelfinavir resistance-conferring mutation D30N on the susceptibility of HIV-1 subtype B to other protease inhibitors.
PMID: 21537677
2011
Memorias do Instituto Oswaldo Cruz
Abstract: Interestingly, in patients with viruses originally containing the D30N mutation who were treated with IDV or SQV, the virus either reversed this mutation or acquired N88D, suggesting an antagonistic effect of D30N upon exposure to these PIs.
Abstract: We demonstrate that D30N increases the susceptibility to saquinavir (SQV) and amprenavir in HIV-1 subtype B isolates and that the N88D mutation in a D30N background neutralizes this effect.
HIV-1 drug resistance at antiretroviral treatment initiation in children previously exposed to single-dose nevirapine.
Result: The major PI mutations M46I/L and I47V were present in 4 samples, and minor PI mutations L10I/V, V11I, A71T, I85V, and N88D were also detected.
Interpretation of genotypic HIV-1 resistance to darunavir and virological response: validation of available systems and of a new score.
Abstract: The DRV-2009 score V11I+L33F+R41K+I47V+2*I50V+2*I54M+K55R+D60E+L74P+L76V+N88D+2*L89V-L10I/V-I13V-G16E-G48V-F53I/L-I62V-I66F-V77I (<0 indicating susceptibility, 0-1 intermediate resistance and >=2 resistance) correlated with VR in the derivation set (n=132, R=0.395; P<0.001).
HIV mutation literature information.
PMID: 
2013
PloS one
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