Discussion: They found that anti-MPER antibodies enhanced the neutralization sensitivity of YU-2 containing the ENF-resistance-conferring mutations G36D or V38 M.
Molecular dynamics studies of the inhibitor C34 binding to the wild-type and mutant HIV-1 gp41: inhibitory and drug resistant mechanism.
Introduction: Now, many mutations are identified, single mutations like G36D/S, V38A/M, Q40H, N42S/T/D/E, N43D/K/S, L44M and L45M have been generally showed to reduce the sensitivity of ENF.
Characterization of Gp41 polymorphisms in the fusion peptide domain and T-20 (Enfuvirtide) resistance-associated regions in Korean HIV-1 isolates.
PMID: 24616600
2014
Journal of Korean medical science
Introduction: T-20 can restrict HIV-1 replication in an efficient manner, but several T-20 resistance mutations have been reported in HR1 as follows: G36D/S, I37V, V38A/M/E, Q39R, Q40H, N42S/T/D/E, N43D/K/S, L44M, L45M, G36S/L44M, G36S/V38M, V38A/N42D, V38A/N42T, V38E/N42S, N42T
Vicriviroc resistance decay and relative replicative fitness in HIV-1 clinical isolates under sequential drug selection pressures.
Abstract: Enfuvirtide was added to the antiretroviral regimen at week 30; by week 48, enfuvirtide treatment selected for either the G36D or N43D HR-1 mutation.
Abstract: This week 48 fitness deficit persisted when G36D was corrected by either site-directed mutagenesis or week 48 gp41 domain swapping.
The binding mode of fusion inhibitor T20 onto HIV-1 gp41 and relevant T20-resistant mechanisms explored by computational study.
Abstract: Based on the T20-gp41 model, seven corresponding structure models of T20-resistant mutants G36D, I37K, V38E, Q39H, Q41R, N43D and L45M were constructed and fully equilibrated by MDS.
Abstract: Besides, mutations G36D, Q39H and L45M only caused minor conformational and energetic changes.
Genotypic analysis of the gp41 HR1 region from HIV-1 isolates from enfuvirtide-treated and untreated patients.
PMID: 21857318
2011
Journal of acquired immune deficiency syndromes (1999)
Abstract: The V38A substitution was the most frequent among treatment-experienced patients followed by the G36D/E, N42D, and V38M substitutions.
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: The V38A (patient C) and N43D (patient D) mutations conferred higher resistance than the G36D (patient C) or N42D+N43S (patient D) mutations respectively, and at intermediate and late time points, the early G36D and
Result: The V38A variant featured 4-fold (full Env) and 6-fold (HR1-HR2) higher resistance than the early G36D clones.
Treatment-mediated alterations in HIV fitness preserve CD4+ T cell counts but have minimal effects on viral load.
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 ENF resistant mutations.
High prevalence of primary Enfuvirtide (ENF) resistance-associated mutations in HIV-1-infected patients in Hong Kong.
Abstract: V69I was found in all samples harboring G36D.
Abstract: G36D was encountered most frequently and more prevalent in non-B subtypes.
Abstract: In three longitudinal samples from an ENF-treated patient, G36D was detected after ENF treatment for 6 months and the mutation persisted after termination of ENF for 6 months.
Abstract: Our findings from the ENF-treated patient showed that G36D mutation persisted as long as 6 months after ENF withdrawal.
Origins of resistance to the HIVgp41 viral entry inhibitor T20.
HIV mutation literature information.
PMID: 
2016
Retrovirology
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