ArticleScientific reports2013
Adhesion and fusion efficiencies of human immunodeficiency virus type 1 (HIV-1) surface proteins.
Article in Scientific reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Nanomechanical characterization of soft nanomaterial using atomic force microscopy.Materials today. Bio · 2025Review
- Biomechanical characterization of SARS-CoV-2 spike RBD and human ACE2 protein-protein interaction.Biophysical journal · 2021Article
- Adhesive contact between cylindrical (Ebola) and spherical (SARS-CoV-2) viral particles and a cell membrane.Mechanics of soft materials · 2020Article
- Biomechanical characterization of TIM protein-mediated Ebola virus-host cell adhesion.Scientific reports · 2019Article
- N-glycan mediated adhesion strengthening during pathogen-receptor binding revealed by cell-cell force spectroscopy.Scientific reports · 2017Article
- Advances in biosensing strategies for HIV-1 detection, diagnosis, and therapeutic monitoring.Advanced drug delivery reviews · 2016Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
In about half of patients infected with HIV-1 subtype B, viral populations shift from utilizing the transmembrane protein CCR5 to CXCR4, as well as or instead of CCR5, during late stage progression of the disease. How the relative adhesion efficiency and fusion competency of the viral Env proteins relate to infection during this transition is not well understood. Using a virus-cell fusion assay and live-cell single-molecule force spectroscopy, we compare the entry competency of viral clones to tensile strengths of the individual Env-receptor bonds of Env proteins obtained from a HIV-1 infected patient prior to and during coreceptor switching. The results suggest that the genetic determinants of viral entry were predominantly enriched in the C3, HR1 and CD regions rather than V3. Env proteins can better mediate entry into cells after coreceptor switch; this effective entry capacity does not correlate with the bond strengths between viral Env and cellular receptors.
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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.