ArticleJournal of virology2006
Role of the envelope genetic context in the development of enfuvirtide resistance in human immunodeficiency virus type 1-infected patients.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 50 citations in OpenAlex.
- Vicriviroc resistance decay and relative replicative fitness in HIV-1 clinical isolates under sequential drug selection pressures.Journal of virology · 2012Trial
- Patterns of genomic site inheritance in HIV-1M inter-subtype recombinants delineate the most likely genomic sites of subtype-specific adaptation.Virus evolution · 2018Article
- HIV-1 diversity in the envelope glycoproteins: implications for viral entry inhibition.Viruses · 2013Review
- Review
- The HR2 polymorphism N140I in the HIV-1 gp41 combined with the HR1 V38A mutation is associated with a less cytopathic phenotype.Retrovirology · 2012Article
- Article
- RNA structures facilitate recombination-mediated gene swapping in HIV-1.Journal of virology · 2010Article
- Identification of a gp41 core-binding molecule with homologous sequence of human TNNI3K-like protein as a novel human immunodeficiency virus type 1 entry inhibitor.Journal of virology · 2010Article
- HIV-1 Entry, Inhibitors, and Resistance.Viruses · 2010Article
- Combinations of the first and next generations of human immunodeficiency virus (HIV) fusion inhibitors exhibit a highly potent synergistic effect against enfuvirtide- sensitive and -resistant HIV type 1 strains.Journal of virology · 2009Article
- Altered bystander apoptosis induction and pathogenesis of enfuvirtide-resistant HIV type 1 Env mutants.AIDS research and human retroviruses · 2009Article
- Molecular mechanisms of recombination restriction in the envelope gene of the human immunodeficiency virus.PLoS pathogens · 2009Article
- HR-2 mutations in human immunodeficiency virus type 1 gp41 restore fusion kinetics delayed by HR-1 mutations that cause clinical resistance to enfuvirtide.Journal of virology · 2009Article
- SC29EK, a peptide fusion inhibitor with enhanced alpha-helicity, inhibits replication of human immunodeficiency virus type 1 mutants resistant to enfuvirtide.Antimicrobial agents and chemotherapy · 2009Article
- Design of peptide-based inhibitors for human immunodeficiency virus type 1 strains resistant to T-20.The Journal of biological chemistry · 2009Article
- Two-way Bayesian hierarchical phylogenetic models: An application to the co-evolution of gp120 and gp41 during and after enfuvirtide treatment.Computational statistics & data analysis · 2009Article
- Peptide P5 (residues 628-683), comprising the entire membrane proximal region of HIV-1 gp41 and its calcium-binding site, is a potent inhibitor of HIV-1 infection.Retrovirology · 2008Article
- Viral dynamics and in vivo fitness of HIV-1 in the presence and absence of enfuvirtide.Journal of acquired immune deficiency syndromes (1999) · 2008Article
- Enfuvirtide antiretroviral therapy in HIV-1 infection.Therapeutics and clinical risk management · 2008Article
- HIV-1 drug-resistance and drug-dependence.Retrovirology · 2007Review
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acquired human immunodeficiency virus type 1(HIV-1) resistance to the fusion inhibitor enfuvirtide (ENF) is primarily associated with mutations within the highly conserved first heptad repeat (HR1) region of gp41. Viral env sequences, however, are remarkably variable, and the envelope genetic background could have an important impact on optimal expression of HR1 mutations. We have examined the genetic evolution of env sequences, ENF susceptibility, and Env replicative capacity in patients failing ENF treatment. Sequential plasma-derived virus populations, obtained from six patients initiating ENF treatment as part of a salvage therapy, were studied using a recombinant phenotypic assay evaluating the entire gp120 and the gp41 ectodomains. Regardless of major differences in the baseline ENF susceptibilities, viral populations with similar phenotypic ENF resistance (50% inhibitory concentration, >3,000 ng/ml) were selected under treatment in four of six patients. As expected, in all patients ENF-resistant viruses harbored one or more HR1 mutations (positions 36, 38, and 43). Interestingly, in five patients the emergence of resistance mutations was not associated with reduced Env replicative capacity. Phylogenetic analysis of env sequences in sequential samples from two patients showed that the HR1 mutations had emerged in the context of env quasi-species that were different from those prevalent at baseline. Thus, the envelope genetic context appears to play a critical role in the selection of HR1 mutations and the expression of ENF resistance, thereby conditioning the evolution of HIV-1 under fusion inhibitor selective pressure.
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