ArticleThe Journal of infectious diseases2015
Analysis of Ebola Virus Entry Into Macrophages.
Article in The Journal of infectious diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 55 citations in OpenAlex.
- Review
- Evaluation of potency and metabolic stability of diphyllin-derived Vacuolar-ATPase inhibitors.European journal of medicinal chemistry · 2024Article
- Molecular insights into the Ebola virus life cycle.Nature microbiology · 2024Review
- Human macrophages infected with Egyptian Rousette bat-isolated Marburg virus display inter-individual susceptibility and antiviral responsiveness.Npj viruses · 2024Article
- Contrasting effects of filamin A and B proteins in modulating filovirus entry.PLoS pathogens · 2023Article
- TIM-1 Augments Cellular Entry of Ebola Virus Species and Mutants, Which Is Blocked by Recombinant TIM-1 Protein.Microbiology spectrum · 2022Article
- Evaluation of Phenol-Substituted Diphyllin Derivatives as Selective Antagonists for Ebola Virus Entry.ACS infectious diseases · 2022Article
- Ebola Virus Entry Inhibitors.Advances in experimental medicine and biology · 2022Article
- Macrophage infection, activation, and histopathological findings in ebolavirus infection.Frontiers in cellular and infection microbiology · 2022Review
- Single virus tracking of Ebola virus entry through lipid rafts in living host cells.Biosafety and health · 2020Article
- Utility of primary cells to examine NPC1 receptor expression in Mops condylurus, a potential Ebola virus reservoir.PLoS neglected tropical diseases · 2020Article
- IL-4/IL-13 polarization of macrophages enhances Ebola virus glycoprotein-dependent infection.PLoS neglected tropical diseases · 2019Article
- Dendritic Cells/Macrophages-Targeting Feature of Ebola Glycoprotein and its Potential as Immunological Facilitator for Antiviral Vaccine Approach.Microorganisms · 2019Review
- Cytokine Effects on the Entry of Filovirus Envelope Pseudotyped Virus-Like Particles into Primary Human Macrophages.Viruses · 2019Article
- Anti-Siglec-1 antibodies block Ebola viral uptake and decrease cytoplasmic viral entry.Nature microbiology · 2019Article
- Anti-Niemann Pick C1 Single-Stranded Oligonucleotides with Locked Nucleic Acids Potently Reduce Ebola Virus Infection In Vitro.Molecular therapy. Nucleic acids · 2019Article
- Characterization of the Filovirus-Resistant Cell Line SH-SY5Y Reveals Redundant Role of Cell Surface Entry Factors.Viruses · 2019Article
- Review of computational methods for virus-host protein interaction prediction: a case study on novel Ebola-human interactions.Briefings in functional genomics · 2018Review
- Ebola Virus Shed Glycoprotein Triggers Differentiation, Infection, and Death of Monocytes Through Toll-Like Receptor 4 Activation.The Journal of infectious diseases · 2018Article
- Ebola virus and persistent chronic infection: when does replication cease?Annals of translational medicine · 2018Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
Ebolaviruses constitute a public health threat, particularly in Central and Western Africa. Host cell factors required for spread of ebolaviruses may serve as targets for antiviral intervention. Lectins, TAM receptor tyrosine kinases (Tyro3, Axl, Mer), T cell immunoglobulin and mucin domain (TIM) proteins, integrins, and Niemann-Pick C1 (NPC1) have been reported to promote entry of ebolaviruses into certain cellular systems. However, the factors used by ebolaviruses to invade macrophages, major viral targets, are poorly defined. Here, we show that mannose-specific lectins, TIM-1 and Axl augment entry into certain cell lines but do not contribute to Ebola virus (EBOV)-glycoprotein (GP)-driven transduction of macrophages. In contrast, expression of Mer, integrin αV, and NPC1 was required for efficient GP-mediated transduction and EBOV infection of macrophages. These results define cellular factors hijacked by EBOV for entry into macrophages and, considering that Mer and integrin αV promote phagocytosis of apoptotic cells, support the concept that EBOV relies on apoptotic mimicry to invade target 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.