A common mechanism of clinical HIV-1 resistance to the CCR5 antagonist maraviroc despite divergent resistance levels and lack of common gp120 resistance mutations.

doi:10.1186/1742-4690-10-43

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

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 - 20 Apr 2013

Roche Michael, Salimi Hamid, Duncan Renee, Wilkinson Brendan L, Chikere Kelechi, Moore Miranda S, Webb Nicholas E, Zappi Helena, Sterjovski Jasminka, Flynn Jacqueline K, Ellett Anne, Gray Lachlan R, Lee Benhur, Jubb Becky, Westby Mike, Ramsland Paul A, Lewin Sharon R, Payne Richard J, Churchill Melissa J, Gorry Paul R

Abstract excerpt

BACKGROUND: The CCR5 antagonist maraviroc (MVC) inhibits human immunodeficiency virus type 1 (HIV-1) entry by altering the CCR5 extracellular loops (ECL), such that the gp120 envelope glycoproteins (Env) no longer recognize CCR5. The mechanisms of HIV-1 resistance to MVC, the only CCR5 antagonist licensed for clinical use are poorly understood, with insights into MVC resistance almost exclusively limited to...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Anti-HIV Agents

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cyclohexanes

Share to HIV-1

Share to HIV Envelope Protein gp120

Share to HIV Infections

Share to Treatment Failure

Share to Triazoles

Share to Virus Internalization

Source

Open in PubMed Open full text

Identifiers

PMID: 23602046
DOI: 10.1186/1742-4690-10-43
PMCID: PMC3648390

Genes

CCR5
MPI

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A common mechanism of clinical HIV-1 resistance to the CCR5 antagonist maraviroc despite divergent resistance levels and lack of common gp120 resistance mutations.PMID 23602046Read ↗

HIV-1 Escape from the CCR5 Antagonist Maraviroc Associated with an Altered and Less-Efficient Mechanism of gp120-CCR5 Engagement That Attenuates Macrophage TropismSemantic proximity Read ↗

Characterizing the Diverse Mutational Pathways Associated with R5-Tropic Maraviroc Resistance: HIV-1 That Uses the Drug-Bound CCR5 CoreceptorSemantic proximity Read ↗

A maraviroc-resistant HIV-1 with narrow cross-resistance to other CCR5 antagonists depends on both N-terminal and extracellular loop domains of drug-bound CCR5.Semantic proximity Read ↗

HIV-1 clinical isolates resistant to CCR5 antagonists exhibit delayed entry kinetics that are corrected in the presence of drug.Semantic proximity Read ↗

HIV-1 Resistance to Maraviroc Conferred by a CD4 Binding Site Mutation in the Envelope Glycoprotein gp120Semantic proximity Read ↗

A pièce de resistance: how HIV-1 escapes small molecule CCR5 inhibitorsSemantic proximity Read ↗

V3-Loop genotypes do not predict maraviroc susceptibility of CCR5-tropic virus or clinical response through week 48 in HIV-1-infected, treatment-experienced persons receiving optimized background regimens.Semantic proximity Read ↗

A single-residue change in the HIV-1 V3 loop associated with maraviroc resistance impairs CCR5 binding affinity while increasing replicative capacitySemantic proximity Read ↗

Detection of HIV-1 CXCR4 tropism and resistance in treatment experienced subjects receiving CCR5 antagonist-Vicriviroc.Semantic proximity Read ↗

Evolution of CCR5 antagonist resistance in an HIV-1 subtype C clinical isolate.Semantic proximity Read ↗

Molecular Gymnastics: Mechanisms of HIV-1 Resistance to CCR5 Antagonists and Impact on Virus Phenotypes.Semantic proximity Read ↗

Reduced maximal inhibition in phenotypic susceptibility assays indicates that viral strains resistant to the CCR5 antagonist maraviroc utilize inhibitor-bound receptor for entry.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.