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 HIV mutation literature information.


  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


  Molecular mechanism of HIV-1 resistance to sifuvirtide, a clinical trial-approved membrane fusion inhibitor.
 PMID: 29929981       2018       The Journal of biological chemistry
Abstract: Importantly, whereas the V38A and Q52R substitutions disrupted the N-terminal helix of gp41, a single A47I substitution greatly enhanced its thermostability.
Abstract: Three primary substitutions (V38A, A47I, and Q52R) located at the inhibitor-binding site of HIV-1's envelope protein (Env) and one secondary substitution (N126K) located at the C-terminal heptad repeat region of the viral protein gp41, which is part of the envelope, conferred high SFT resistance and cross-resistance to the anti-HIV-1 drug T20 and the template peptide C34.
Abstract: We fo


  Enhanced antibody-mediated neutralization of HIV-1 variants that are resistant to fusion inhibitors.
 PMID: 27670680       2016       Retrovirology
Result: For comparison with other fusion inhibitor resistant mutants, we selected three ENF resistant mutants V38A, Q40H, and N43D, because these mutations were frequently observed in ENF treated patients and confer more than tenfold resistance to ENF.
Result: In contrast, two of the three mutations conferring ENF resistance, V38A and Q40H, were unable to affect the neutralization sensitivity by these antibodies.
Result: Two ENF-resistant mutants, N43D and Q40H, showed low infectivity compared with WT (approximately tenfold), but the infectivity of the V38A mutant was at the same level as the WT.


  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


  Molecular dynamics studies of the inhibitor C34 binding to the wild-type and mutant HIV-1 gp41: inhibitory and drug resistant mechanism.
 PMID: 25393106       2014       PloS one
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.


  The HR2 polymorphism N140I in the HIV-1 gp41 combined with the HR1 V38A mutation is associated with a less cytopathic phenotype.
 PMID: 22333046       2012       Retrovirology
Abstract: CONCLUSIONS: Overall, primary gp41 proteins with both V38A and N140I changes showed a reduced ability to induce single cell death and deplete CD4+ T cells, despite maintaining fusion activity.
Abstract: Conversely, Env acquiring the V38A mutation in a 140I background induced a significantly reduced loss of CD4+ T cells and lower single-cell death than did their baseline controls.
Abstract: To test this hypothesis, we have characterized the expression, fusion capability, induction of CD4+ T cell loss and single CD4+ T cell death of 48 gp41 proteins derived from three patients displaying different amino acids (N, T or I) at position 140 that developed a V38A mutation after ENF-based treatment.


  Genetic and structural analysis of HIV-1 Rev responsive element related to V38A and T18A enfuvirtide resistance mutations.
 PMID: 22188777       2012       Intervirology
Abstract: METHODS: Collecting 476 and 135 HIV-1 B-subtype gp41 sequences from enfuvirtide-naive and enfuvirtide-treated patients, respectively, two mutations previously found associated with enfuvirtide treatment, T18A and V38A, were analyzed.
Abstract: We previously found the co-presence of V38A+T18A resistance mutations in patients failing enfuvirtide.
Abstract: While a structural RRE impairment in the presence of V38A alone was found, a restoration of the original RRE structure occurred in co-presence of V38A+T18A.


  HIV type 1 molecular epidemiology in pol and gp41 genes among naive patients from Mato Grosso do Sul State, central western Brazil.
 PMID: 21790471       2012       AIDS research and human retroviruses
Abstract: T-20/gp41 resistance mutations were L44M (n=2) and V38A (n=1).


  Increasing hydrophobicity of residues in an anti-HIV-1 Env peptide synergistically improves potency.
 PMID: 21504732       2011       Biophysical journal
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.


  Dynamics of enfuvirtide resistance mutations in enfuvirtide-experienced patients remaining in virological failure under salvage therapy.
 PMID: 21341978       2011       Scandinavian journal of infectious diseases
Abstract: RESULTS: Genotypic profiles of ENF-resistant variants at ENF discontinuation were as follows: V38A in 3 patients, V38A+N42T+N43D in 1 patient, N43D in 2 patients, and N43K in 1 patient.



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