Daphnane Diterpenoids from Trigonostemon lii and Inhibition Activities Against HIV-1.
PMID: 32048186
2020
Natural products and bioprospecting
Abstract: Moreover, all of the diterpenoids shows significant inhibitions against T20-resistan HIV-1 strains, PNL4-3gp41(36G)V38E, N42S and pNL4-3gp41(36G)V38A, N42T.
Introduction: More important, these compounds still displayed significant inhibitions against T20-resistant HIV-1 strains, pNL4-3gp41(36G)V38E, N42S and pNL4-3gp41(36G)V38A, N42T.
Result: It not only inhibited replication of HIV-1 laboratory strains (HIV-1IIIB), but also inhibited T20-resistant strains (pNL4-3gp41(36G)V38E,N42S and pNL4-3gp41(36G)V38A,N42T) that those compounds showed strong inhibitory activiti
Structural and Thermodynamic Analysis of HIV-1 Fusion Inhibition Using Small gp41 Mimetic Proteins.
Abstract: Here, we investigated two covNHR variants differing in two mutations, V10E and Q123R (equivalent to V38E and Q40R in gp41 sequence) that reproduce the effect of HIV-1 mutations associated with resistance to fusion inhibitors, such as T20 (enfuvirtide).
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
The HR2 polymorphism N140I in the HIV-1 gp41 combined with the HR1 V38A mutation is associated with a less cytopathic phenotype.
Result: Because there were no significant differences in fusogenicity among the Envs tested in our assays, we specifically quantified Env-mediated cell death, since in vitro the single-amino-acid mutation V38A/E has been shown to alter this mechanism.
Result: In agreement with this property, it has been described that single-amino-acid mutations in the ectodomain (V38A/E) or transmembrane regions of gp41 reduce cell-to-cell fusion activity of the virus.
The binding mode of fusion inhibitor T20 onto HIV-1 gp41 and relevant T20-resistant mechanisms explored by computational study.
Abstract: Also notably, the V38E and N43D mutations hindered the binding of T20 through electrostatic repulsion and thus also resulted in dramatic change in binding energy.
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.
Single amino acid change in gp41 region of HIV-1 alters bystander apoptosis and CD4 decline in humanized mice.
Abstract: Interestingly, immune activation was observed with both WT and V38E infection suggesting that the two phenomena are likely not interdependent in the mouse model.
Abstract: This differential pathogenesis was associated with a lack of bystander apoptosis induction by V38E virus even in the presence of similar levels of infected cells.
Abstract: We demonstrate here that a single amino acid change (V38E) altering the cell-to-cell fusion activity of the Env minimizes CD4 loss in humanized mice without altering viral replication.
Introduction: Using this virus as a model system, in this study, we have compared the pathogenicity of WT and V38E mutant in the humanized mice and find that while both viruses replicate to similar levels and induce immune activation, V38E
Origins of resistance to the HIVgp41 viral entry inhibitor T20.
Abstract: (2) Charged mutations (I37K, Q40K, and V38E) lead to significant Coulombic changes that weaken favorable van der Waals interactions.
Abstract: In addition, seven deleterious gp41 point mutations (L33Q, L33S, G36V, I37K, V38E, Q40H, and Q40K) were simulated, and all correctly exhibited decreases in the level of binding, including the fact that L33Q and Q40K are most detrimental.
Introduction: Mutations at sites L33Q, V38E, Q40K
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.
Enfuvirtide (T-20) resistance-related mutations in HIV type 1 subtypes B, C, and F isolates from Brazilian patients failing HAART.
PMID: 19239358
2009
AIDS research and human retroviruses
Abstract: Amino acid changes in codons G36D/S, I37V, V38A/M/E, Q39H/R, Q40H, N42T, and N43D can confer resistance to EFV.
Human immunodeficiency virus type 1 gp 41 mutations in proviral DNA among antiretroviral treatment-naive individuals from India.
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: 
2020
Natural products and bioprospecting
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