Abstract: V38A did not substantially reduce infectivity, but was relatively resistant to inhibitory peptides.
Abstract: In this study, ENF-resistant mutants--V38A, N43D, N43D/S138A, Q40H/L45M--were combined with modified inhibitory peptides to identify what we believe to be novel ways to improve peptide efficacy.
Impact of the HIV-1 env genetic context outside HR1-HR2 on resistance to the fusion inhibitor enfuvirtide and viral infectivity in clinical isolates.
Abstract: All escape clones carried at least one of G36D, V38A, N42D and/or N43D/S in HR1, and accordingly, resistance increased 11- to 2800-fold relative to baseline.
Result: At later time points, only the V38A mutation was detected associated with the L44M resistance mutation.
Result: For patient C, 4/5 early escape viruses carried the G36D substitution and one clone carried the V38A mutation.
Result: For patient C, all late (week 129) clones were extremely tightly related and emerged from the branch grouping early G36D variants (clones 27.3, 27.4, 27.6) rather than from the early V38A variant or from the intermediate
Treatment-mediated alterations in HIV fitness preserve CD4+ T cell counts but have minimal effects on viral load.
Abstract: Focusing on resistant viruses carrying the V38A mutation in gp41, we found ENF-resistant virus to be 17+-3% less fit than ENF-sensitive virus in the absence of the drug, and that the loss of resistant virus during therapy interruption was primarily due to this fitness cost.
Introduction: Resistance to ENF occurs due to amino acid substitutions within the HR-1 region of gp41 at amino acids 36-45 of HIV-1 gp41 with G36D, G36S, G36V, G36E, V38A, V38M, V38E, Q40H, N42T, and N43D being the most common
Resistance profiles of novel electrostatically constrained HIV-1 fusion inhibitors.
PMID: 20937812
2010
The Journal of biological chemistry
Abstract: However, the efficacy of T-20 is attenuated by resistance mutations in gp41, including V38A and N43D.
Origins of resistance to the HIVgp41 viral entry inhibitor T20.
Short communication: Simultaneous substitutions of V38M and N43T-N44K in the gp41 heptad repeat 1 (HR1) disrupt HIV type 1 gPr160 endoproteolytic cleavage (*).
PMID: 20055586
2010
AIDS research and human retroviruses
Abstract: Two mutations, a single V38A and a double N43T-N44K were the most frequent; however, they were not found together in one clone.
Altered bystander apoptosis induction and pathogenesis of enfuvirtide-resistant HIV type 1 Env mutants.
PMID: 19619009
2009
AIDS research and human retroviruses
Abstract: The viruses were found to have apoptosis-inducing activity in the order WT > V38M > V38A > G36D > V38E, which correlated with cell-to-cell fusion but not infection.
Introduc
Introduction: As seen in figure 4, V38E and V38A along with G36D replicated faster and to higher levels than WT.
Introduction: The degree of resistance was in the order WT<V38M< G36D<V38A<V38E (Table 1).
Introduction: The order of apoptosis induction was WT>V38M>V38A>G36D>V38E.
In vivo selection by enfuvirtide of HIV type-1 env quasispecies with optimal potential for phenotypic expression of HR1 mutations.
Abstract: Back-mutation of V38A from these clones resulted in a strong loss in ENF resistance, but these clones retained significant residual resistance, again strongly suggesting the role of determinants outside of HR1 in HIV-1 resistance to ENF.
Abstract: RESULTS: The ENF resistance levels produced by the introduction of mutation V38A in pretherapeutic env sequences were significantly lower than those of env clones harvested after viral escape, and in which V38A was naturally selected.
Analysis of HIV type 1 gp41 and enfuvirtide susceptibility among men in the United States who were HIV infected prior to availability of HIV entry inhibitors.
PMID: 19552592
2009
AIDS research and human retroviruses
Introduction: The mutations analyzed included (1) mutations in HR1 that are associated with a >10-fold reduction in most clinical isolates and site-directed mutants (major mutations: G36D/E, V38A/E, Q40H, and N43D), (2) other ENF resistance mutations in HR1 (G36S/V, I37V, V38G/M, N42T, N43K, L44M, and L45M), (3) N42S, a natural polymorphism in HR1 that has been associated with ENF hypersusceptibility, and (4) HR2 accessory mutations (N126K, E137K, and S138A).
Table: PMID: 19400735
2009
AIDS research and human retroviruses
Abstract: In subtype B-infected individuals, the various HR1 region substitutions in env gp41 that have been associated with ENF resistance include A30V, L33S/T/V, L34M, G36D/E/S/V, I37T/K/V, V38A/M/E/G, Q39R, Q40H, N42T/D, N43D/K/S, L44M, L45M, R46M, L54M, and Q56K/R as well as N126K and
HIV mutation literature information.
PMID: 
2011
Biophysical journal
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