ArticlePLoS pathogens2008
Phosphoinositide-3 kinase-Akt pathway controls cellular entry of Ebola virus.
Article in PLoS pathogens, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.
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Who cites it
122 citing papers in PubMed, 194 citations in OpenAlex.
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- Cilnidipine exerts antiviral effects in vitro and in vivo by inhibiting the internalization and fusion of influenza A virus.BMC medicine · 2025Article
- Multiple cell types support productive infection and dynamic translocation of infectious Ebola virus to the surface of human skin.Science advances · 2025Article
- Inositol metabolism as a broad-spectrum antiviral target.Frontiers in microbiology · 2025Review
- Screening of neurotransmitter receptor modulators reveals novel inhibitors of influenza virus replication.Frontiers in cellular and infection microbiology · 2025Article
- Reduced insulin/IGF-1 signalling upregulates two anti-viral immune pathways, decreases viral load and increases survival under viral infection in C. elegans.GeroScience · 2024Article
- Proteomics Analysis of Duck Lung Tissues in Response to Highly Pathogenic Avian Influenza Virus.Microorganisms · 2024Article
- Identification and Potential Roles of Human MicroRNAs in Ebola Virus Infection and Disease Pathogenesis.Genes · 2024Article
- Navigating the Complex Landscape of Ebola Infection Treatment: A Review of Emerging Pharmacological Approaches.Infectious diseases and therapy · 2024Review
- Transcriptome analysis of salivary glands of rabies-virus-infected mice.Frontiers in microbiology · 2024Article
- Role of Virus-Induced EGFR Trafficking in Proviral Functions.Biomolecules · 2023Review
- The Small GTPase Rab14 Regulates the Trafficking of Ceramide from Endoplasmic Reticulum to Golgi Apparatus and Facilitates Classical Swine Fever Virus Assembly.Journal of virology · 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
- Targeting Human Proteins for Antiviral Drug Discovery and Repurposing Efforts: A Focus on Protein Kinases.Viruses · 2023Review
- 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
- PI3K/Akt/Nrf2 mediated cellular signaling and virus-host interactions: latest updates on the potential therapeutic management of SARS-CoV-2 infection.Frontiers in molecular biosciences · 2023Review
- PIK-24 Inhibits RSV-Induced Syncytium Formation via Direct Interaction with the p85α Subunit of PI3K.Journal of virology · 2022Article
- Filoviruses: Innate Immunity, Inflammatory Cell Death, and Cytokines.Pathogens (Basel, Switzerland) · 2022Review
- Live and let die: signaling AKTivation and UPRegulation dynamics in SARS-CoVs infection and cancer.Cell death & disease · 2022Review
62 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The phosphoinositide-3 kinase (PI3K) pathway regulates diverse cellular activities related to cell growth, migration, survival, and vesicular trafficking. It is known that Ebola virus requires endocytosis to establish an infection. However, the cellular signals that mediate this uptake were unknown for Ebola virus as well as many other viruses. Here, the involvement of PI3K in Ebola virus entry was studied. A novel and critical role of the PI3K signaling pathway was demonstrated in cell entry of Zaire Ebola virus (ZEBOV). Inhibitors of PI3K and Akt significantly reduced infection by ZEBOV at an early step during the replication cycle. Furthermore, phosphorylation of Akt-1 was induced shortly after exposure of cells to radiation-inactivated ZEBOV, indicating that the virus actively induces the PI3K pathway and that replication was not required for this induction. Subsequent use of pseudotyped Ebola virus and/or Ebola virus-like particles, in a novel virus entry assay, provided evidence that activity of PI3K/Akt is required at the virus entry step. Class 1A PI3Ks appear to play a predominant role in regulating ZEBOV entry, and Rac1 is a key downstream effector in this regulatory cascade. Confocal imaging of fluorescently labeled ZEBOV indicated that inhibition of PI3K, Akt, or Rac1 disrupted normal uptake of virus particles into cells and resulted in aberrant accumulation of virus into a cytosolic compartment that was non-permissive for membrane fusion. We conclude that PI3K-mediated signaling plays an important role in regulating vesicular trafficking of ZEBOV necessary for cell entry. Disruption of this signaling leads to inappropriate trafficking within the cell and a block in steps leading to membrane fusion. These findings extend our current understanding of Ebola virus entry mechanism and may help in devising useful new strategies for treatment of Ebola virus infection.
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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.