ArticleThe Journal of infectious diseases2018
Autophagy-Associated Proteins Control Ebola Virus Internalization Into Host Cells.
Article in The Journal of infectious diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 23 citations in OpenAlex.
- Discovering host-viral protein interactions in autophagy: A LIR discovery pipeline for identifying LC3-interacting region motifs in highly virulent viruses.PLoS pathogens · 2026Article
- SIRT5 Inhibits Mitophagy and Inflammation of Hypoxia-Induced Pulmonary Hypertension by Regulating the Desuccinylation of PDK1.Molecular biotechnology · 2026Article
- Autophagy in emerging and highly concerned severe zoonotic infectious diseases.Frontiers in immunology · 2026Review
- Host-Microbe Interactions: Understanding the Mechanism of Autophagy in Viral Replication and Immune Evasion.Veterinary sciences · 2025Review
- Article
- Genome-wide CRISPR/Cas9 screen identifies SLC39A9 and PIK3C3 as crucial entry factors for Ebola virus infection.PLoS pathogens · 2024Article
- Coordinated inflammatory responses dictate Marburg virus control by reservoir bats.Nature communications · 2024Article
- Ebola Virus Uses Tunneling Nanotubes as an Alternate Route of Dissemination.The Journal of infectious diseases · 2023Article
- Contrasting effects of filamin A and B proteins in modulating filovirus entry.PLoS pathogens · 2023Article
- Sphingosine Kinases Promote Ebola Virus Infection and Can Be Targeted to Inhibit Filoviruses, Coronaviruses, and Arenaviruses Using Late Endocytic Trafficking to Enter Cells.ACS infectious diseases · 2023Article
- Chaperone-assisted selective autophagy targets filovirus VP40 as a client and restricts egress of virus particles.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Review
- Factors affecting RIG-I-Like receptors activation - New research direction for viral hemorrhagic fevers.Frontiers in immunology · 2022Review
- Article
- Placental Autophagy and Viral Replication Co-localize in Human and Non-human Primate Placentae Following Zika Virus Infection: Implications for Therapeutic Interventions.Frontiers in virology (Lausanne, Switzerland) · 2021Article
- Frontline Science: CD40 signaling restricts RNA virus replication in Mϕs, leading to rapid innate immune control of acute virus infection.Journal of leukocyte biology · 2021Article
- Immunological Perspective for Ebola Virus Infection and Various Treatment Measures Taken to Fight the Disease.Pathogens (Basel, Switzerland) · 2020Review
- Filoviruses Use the HOPS Complex and UVRAG To Traffic to Niemann-Pick C1 Compartments during Viral Entry.Journal of virology · 2020Article
- Acute Plasmodium Infection Promotes Interferon-Gamma-Dependent Resistance to Ebola Virus Infection.Cell reports · 2020Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Ebola virus (EBOV) enters host cells by macropinocytosis, a poorly understood process. Recent studies have suggested that cell factors involved in autophagy, an evolutionally conserved pathway leading to the lysosomal degradation of protein aggregates and organelles during cellular stress, also have roles in macropinocytosis. Here, we demonstrate that autophagy-associated proteins are required for trafficking of EBOV into the cell body. Depleting cells of beclin 1, autophagy-related protein 7, or microtubule-associated protein 1A/B light chain 3B (LC3B) abolished EBOV uptake, owing to a block in vesicle formation at the cell surface. Both LC3B-I and LC3B-II interacted with macropinocytic structures. Our work indicates that, although various forms of LC3B possess an inherent ability to associate with forming macropinosomes, LC3B-II is critical for internalization of macropinocytic vesicles and, therefore, EBOV from the cell surface.
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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.