ArticleJournal of virology2015
Suppressor of Cytokine Signaling 3 Is an Inducible Host Factor That Regulates Virus Egress during Ebola Virus Infection.
Article in Journal of virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- Article
- Immunoinformatic-driven design and evaluation of multi-epitope mRNA vaccine targeting HIV-1 gp120.Frontiers in immunology · 2025Article
- Molecular insights into the Ebola virus life cycle.Nature microbiology · 2024Review
- Activation of TLR4 by viral glycoproteins: A double-edged sword?Frontiers in microbiology · 2022Review
- Article
- Targeted Profiling of Immunological Genes during Norovirus Replication in Human Intestinal Enteroids.Viruses · 2021Article
- HER2-mediated enhancement of Ebola virus entry.PLoS pathogens · 2020Article
- Unpuzzling COVID-19: tissue-related signaling pathways associated with SARS-CoV-2 infection and transmission.Clinical science (London, England : 1979) · 2020Article
- Coxsackievirus B3 Infection of Human Neural Progenitor Cells Results in Distinct Expression Patterns of Innate Immune Genes.Viruses · 2020Article
- Zika Virus-Induction of the Suppressor of Cytokine Signaling 1/3 Contributes to the Modulation of Viral Replication.Pathogens (Basel, Switzerland) · 2020Article
- Porcine Reproductive and Respiratory Syndrome Virus Enhances Self-Replication via AP-1-Dependent Induction of SOCS1.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Single-walled carbon nanotubes repress viral-induced defense pathways through oxidative stress.Nanotoxicology · 2019Article
- Review
- Review
- Toll-like receptor 4 in acute viral infection: Too much of a good thing.PLoS pathogens · 2018Review
- LY6E mediates an evolutionarily conserved enhancement of virus infection by targeting a late entry step.Nature communications · 2018Article
- Immune barriers of Ebola virus infection.Current opinion in virology · 2018Review
- A review on the antagonist Ebola: A prophylactic approach.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2017Review
- Ebolaviruses Associated with Differential Pathogenicity Induce Distinct Host Responses in Human Macrophages.Journal of virology · 2017Article
- Immunobiology of Ebola and Lassa virus infections.Nature reviews. Immunology · 2017Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
unlabelledEbola virus (EBOV) initially targets monocytes and macrophages, which can lead to the release of proinflammatory cytokines and chemokines. These inflammatory cytokines are thought to contribute to the development of circulatory shock seen in fatal EBOV infections. The VP40 matrix protein is a key viral structural protein that is critical for virion egress. Physical and functional interactions between VP40 and host proteins such as Tsg101 and Nedd4 facilitate efficient release of VP40-driven virus-like particles (VLPs) and infectious virus. Here, we show that host suppressor of cytokine signaling 3 (SOCS3) can also bind to EBOV VP40, leading to enhanced ubiquitinylation and egress of VP40. Indeed, titers of infectious EBOV derived from SOCS3 knockout mouse embryonic fibroblasts (MEFs) were significantly reduced compared to those from wild-type (WT) MEFs at 24 and 48 h postinfection. Importantly, this reduced virus yield could be rescued back to WT levels by exogenously expressing SOCS3. Lastly, we show that SOCS3 expression is induced by EBOV glycoprotein (GP) expression and that VLPs containing EBOV VP40 and GP induced production of proinflammatory cytokines, which induced SOCS3 for negative-feedback regulation. These data indicate that host innate immune protein SOCS3 may play an important role in budding and pathogenesis of EBOV. IMPORTANCE: The VP40 matrix protein is a key structural protein critical for Ebola virus budding. Physical and functional interactions between VP40 and host proteins such as Tsg101 and Nedd4 facilitate efficient release of VLPs and infectious virus. We reported that host TLR4 is a sensor for Ebola GP on VLPs and that the resultant TLR4 signaling pathways lead to the production of proinflammatory cytokines. Host SOCS3 regulates the innate immune response by controlling and limiting the proinflammatory response through negative-feedback inhibition of cytokine receptors. We present evidence that Ebola virus VLPs stimulate induction of SOCS3 as well as proinflammatory cytokines, and that expression of human SOCS3 enhances budding of Ebola VLPs and infectious virus via a mechanism linked to the host ubiquitinylation machinery.
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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.