ArticleJournal of virology2011
Cross-linking of rotavirus outer capsid protein VP7 by antibodies or disulfides inhibits viral entry.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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.
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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
14 citing papers in PubMed, 31 citations in OpenAlex.
- Cross-Neutralizing and Broadly Neutralizing Human Antibodies Against Nonenveloped Viruses.European journal of immunology · 2026Review
- Cross-neutralization and antigenic characterization of simian and equine group A rotaviruses.Journal of virology · 2026Article
- Mechanism of membrane perforation in rotavirus cell entry.bioRxiv : the preprint server for biology · 2026Article
- Deep learning-assisted analysis of single-particle tracking for automated correlation between diffusion and function.Nature methods · 2025Article
- Spectroscopic analysis of the bacterially expressed head domain of rotavirus VP6.Bioscience reports · 2024Article
- Monoreassortant Rotaviruses of Multiple G Types Are Differentially Neutralized by Sera From Infants Vaccinated With ROTARIX and RotaTeq.The Journal of infectious diseases · 2021Article
- Multiple Introductions and Antigenic Mismatch with Vaccines May Contribute to Increased Predominance of G12P[8] Rotaviruses in the United States.Journal of virology · 2019Article
- Visualization of Calcium Ion Loss from Rotavirus during Cell Entry.Journal of virology · 2018Article
- VP4- and VP7-specific antibodies mediate heterotypic immunity to rotavirus in humans.Science translational medicine · 2017Article
- Fusion of the mouse IgG1 Fc domain to the VHH fragment (ARP1) enhances protection in a mouse model of rotavirus.Scientific reports · 2016Article
- Structural plasticity of the coiled-coil domain of rotavirus NSP4.Journal of virology · 2014Article
- Structural correlates of rotavirus cell entry.PLoS pathogens · 2014Article
- Rotavirus activates lymphocytes from non-obese diabetic mice by triggering toll-like receptor 7 signaling and interferon production in plasmacytoid dendritic cells.PLoS pathogens · 2014Article
- Structural and functional basis for inhibition of erythrocyte invasion by antibodies that target Plasmodium falciparum EBA-175.PLoS pathogens · 2013Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Antibodies that neutralize rotavirus infection target outer coat proteins VP4 and VP7 and inhibit viral entry. The structure of a VP7-Fab complex (S. T. Aoki, et al., Science 324:1444-1447, 2009) led us to reclassify epitopes into two binding regions at inter- and intrasubunit boundaries of the calcium-dependent trimer. It further led us to show that antibodies binding at the intersubunit boundary inhibit uncoating of the virion outer layer. We have now tested representative antibodies for each of the defined structural epitope regions and find that antibodies recognizing epitopes in either binding region neutralize by cross-linking VP7 trimers. Antibodies that bind at the intersubunit junction neutralize as monovalent Fabs, while those that bind at the intrasubunit region require divalency. The VP7 structure has also allowed us to design a disulfide cross-linked VP7 mutant which recoats double-layered particles (DLPs) as efficiently as does wild-type VP7 but which yields particles defective in cell entry as determined both by lack of infectivity and by loss of α-sarcin toxicity in the presence of recoated particles. We conclude that dissociation of the VP7 trimer is an essential step in viral penetration into cells.
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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.