ArticleThe Journal of infectious diseases2007
Analysis of the interaction of Ebola virus glycoprotein with DC-SIGN (dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin) and its homologue DC-SIGNR.
Article in The Journal of infectious diseases, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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.
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Who cites it
55 citing papers in PubMed, 86 citations in OpenAlex.
- Elucidating genes sufficient for viral entry into cells through sequential genome-wide CRISPR activation screens.bioRxiv : the preprint server for biology · 2026Article
- Article
- Molecular determinants of cross-species transmission in emerging viral infections.Microbiology and molecular biology reviews : MMBR · 2024Review
- Molecular insights into the Ebola virus life cycle.Nature microbiology · 2024Review
- Human Milk Oligosaccharide 2'-Fucosyllactose Inhibits Ligand Binding to C-Type Lectin DC-SIGN but Not to Langerin.International journal of molecular sciences · 2022Article
- Filoviruses: Innate Immunity, Inflammatory Cell Death, and Cytokines.Pathogens (Basel, Switzerland) · 2022Review
- TIM-1 Augments Cellular Entry of Ebola Virus Species and Mutants, Which Is Blocked by Recombinant TIM-1 Protein.Microbiology spectrum · 2022Article
- Human surfactant protein D facilitates SARS-CoV-2 pseudotype binding and entry in DC-SIGN expressing cells, and downregulates spike protein induced inflammation.Frontiers in immunology · 2022Article
- Glycan-Lectin Interactions in Cancer and Viral Infections and How to Disrupt Them.International journal of molecular sciences · 2021Review
- C-type lectins and extracellular vesicles in virus-induced NETosis.Journal of biomedical science · 2021Review
- DC/L-SIGN recognition of spike glycoprotein promotes SARS-CoV-2 trans-infection and can be inhibited by a glycomimetic antagonist.PLoS pathogens · 2021Article
- Identification of Important N-Linked Glycosylation Sites in the Hemagglutinin Protein and Their Functional Impact on DC-SIGN Mediated Avian Influenza H5N1 Infection.International journal of molecular sciences · 2021Article
- Interaction Between Virus-Like Particles (VLPs) and Pattern Recognition Receptors (PRRs) From Dendritic Cells (DCs): Toward Better Engineering of VLPs.Frontiers in immunology · 2020Review
- Dendritic Cells/Macrophages-Targeting Feature of Ebola Glycoprotein and its Potential as Immunological Facilitator for Antiviral Vaccine Approach.Microorganisms · 2019Review
- A Critical Domain of Ebolavirus Envelope Glycoprotein Determines Glycoform and Infectivity.Scientific reports · 2018Article
- Review
- Review
- Anti-Ebola therapies based on monoclonal antibodies: current state and challenges ahead.Critical reviews in biotechnology · 2017Review
- Filovirus proteins for antiviral drug discovery: A structure/function analysis of surface glycoproteins and virus entry.Antiviral research · 2016Review
- DC-SIGN and L-SIGN Are Attachment Factors That Promote Infection of Target Cells by Human Metapneumovirus in the Presence or Absence of Cellular Glycosaminoglycans.Journal of virology · 2016Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe lectin DC-SIGN (dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin) augments Ebola virus (EBOV) infection. However, it its unclear whether DC-SIGN promotes only EBOV attachment (attachment factor function, nonessential) or actively facilitates EBOV entry (receptor function, essential).
methodsWe investigated whether DC-SIGN on B cell lines and dendritic cells acts as an EBOV attachment factor or receptor.
resultsEngineered DC-SIGN expression rendered some B cell lines susceptible to EBOV glycoprotein (EBOV GP)-driven infection, whereas others remained refractory, suggesting that cellular factors other than DC-SIGN are also required for susceptibility to EBOV infection. Augmentation of entry was independent of efficient DC-SIGN internalization and might not involve lectin-mediated endocytic uptake of virions. Therefore, DC-SIGN is unlikely to function as an EBOV receptor on B cell lines; instead, it might concentrate virions onto cells, thereby allowing entry into cell lines expressing low levels of endogenous receptor(s). Indeed, artificial concentration of virions onto cells mirrored DC-SIGN expression, confirming that optimization of viral attachment is sufficient for EBOV GP-driven entry into some B cell lines. Finally, EBOV infection of dendritic cells was only partially dependent on mannose-specific lectins, such as DC-SIGN, suggesting an important contribution of other factors.
conclusionsOur results indicate that DC-SIGN is not an EBOV receptor but, rather, is an attachment-promoting factor that boosts entry into B cell lines susceptible to low levels of EBOV GP-mediated infection.
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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.