ArticleVirology2012
V3 determinants of HIV-1 escape from the CCR5 inhibitors Maraviroc and Vicriviroc.
Article in Virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed.
- The clinical potential of gene editing as a tool to engineer cell-based therapeutics.Clinical and translational medicine · 2020Review
- Prevalence of CCR5delta32 in Northeastern Iran.BMC medical genetics · 2019Article
- Phenotypic co-receptor tropism and Maraviroc sensitivity in HIV-1 subtype C from East Africa.Scientific reports · 2018Article
- Article
- HIV-1 Group O Genotypes and Phenotypes: Relationship to Fitness and Susceptibility to Antiretroviral Drugs.AIDS research and human retroviruses · 2016Article
- Incompatible Natures of the HIV-1 Envelope in Resistance to the CCR5 Antagonist Cenicriviroc and to Neutralizing Antibodies.Antimicrobial agents and chemotherapy · 2016Article
- A single-residue change in the HIV-1 V3 loop associated with maraviroc resistance impairs CCR5 binding affinity while increasing replicative capacity.Retrovirology · 2015Article
- Maraviroc: a review of its use in HIV infection and beyond.Drug design, development and therapy · 2015Review
- Complexity and dynamics of HIV-1 chemokine receptor usage in a multidrug-resistant adolescent.AIDS research and human retroviruses · 2014Article
- Synergistic combinations of the CCR5 inhibitor VCH-286 with other classes of HIV-1 inhibitors.Antimicrobial agents and chemotherapy · 2014Article
- Review
- Analysis of primary resistance mutations to HIV-1 entry inhibitors in therapy naive subtype C HIV-1 infected mother-infant pairs from Zambia.Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology · 2013Article
- Mutations in variable domains of the HIV-1 envelope gene can have a significant impact on maraviroc and vicriviroc resistance.AIDS research and therapy · 2013Article
- Use of G-protein-coupled and -uncoupled CCR5 receptors by CCR5 inhibitor-resistant and -sensitive human immunodeficiency virus type 1 variants.Journal of virology · 2013Article
- Review
- A common mechanism of clinical HIV-1 resistance to the CCR5 antagonist maraviroc despite divergent resistance levels and lack of common gp120 resistance mutations.Retrovirology · 2013Article
- Structure and dynamics of the gp120 V3 loop that confers noncompetitive resistance in R5 HIV-1(JR-FL) to maraviroc.PloS one · 2013Article
- Review
- Effects of sequence changes in the HIV-1 gp41 fusion peptide on CCR5 inhibitor resistance.Virology · 2012Article
Corrections and comments
- Erratum issuedJakobsen, Martin R [added]; Gorry, Paul R [added]
Authors and funding
6 authors.
Funding
Abstract
HIV-1 develops resistance to CCR5 antagonists such as Maraviroc (MVC) and Vicriviroc (VVC) both in vitro and in vivo, with most changes arising in the gp120 V3 region. Both compounds bind to the same hydrophobic cavity in CCR5 in subtly different ways. Here, we investigated which V3 sequence changes are most associated with MVC and VVC resistance and how they affect the interaction between gp120 and the CCR5 NT. We found that VVC- and MVC-selected amino acid changes map to different V3 locations and involve residues that interact with the CCR5 NT in different ways. Changes in VVC-selected, but not MVC-selected, variants often involve charged residues. Although the overall V3 charge tends not to change, the introduction or removal of charged residues at specific positions affects the local electrostatic potential and could have structural and functional implications. In summary, VVC and MVC trigger the evolution of distinct HIV-1 resistance patterns in V3.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.