ArticleBMC genomics2016
In vivo Ebola virus infection leads to a strong innate response in circulating immune cells.
Article in BMC genomics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed.
- Nanobody targeting glycan cap confers broad orthoebolavirus neutralization.Virologica Sinica · 2026Article
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- Superior replication, pathogenicity, and immune evasion of a Texas dairy cattle H5N1 virus compared to a historical avian isolate.Scientific reports · 2025Article
- Droplet-Based Single-Cell 3' mRNA Sequencing of Marburg Virus-Infected Samples.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Machine learning-based analysis of Ebola virus' impact on gene expression in nonhuman primates.Frontiers in artificial intelligence · 2024Article
- Natural history of Ebola virus disease in rhesus monkeys shows viral variant emergence dynamics and tissue-specific host responses.Cell genomics · 2023Article
- Understanding virus-host interactions in tissues.Nature microbiology · 2023Review
- Single-cell profiling of lncRNA expression during Ebola virus infection in rhesus macaques.Nature communications · 2023Article
- Peripheral immune responses to filoviruses in a reservoir versus spillover hosts reveal transcriptional correlates of disease.Frontiers in immunology · 2023Article
- Ebola virus infection induces a delayed type I IFN response in bystander cells and the shutdown of key liver genes in human iPSC-derived hepatocytes.Stem cell reports · 2022Article
- Treatment with Ad5-Porcine Interferon-α Attenuates Ebolavirus Disease in Pigs.Pathogens (Basel, Switzerland) · 2022Article
- Different but Not Unique: Deciphering the Immunity of the Jamaican Fruit Bat by Studying Its Viriome.Viruses · 2022Review
- Heterogeneity in the Response of Different Subtypes ofViruses · 2021Article
- Interferon-Induced HERC5 Inhibits Ebola Virus Particle Production and Is Antagonized by Ebola Glycoprotein.Cells · 2021Article
- Article
- HERC5 and the ISGylation Pathway: Critical Modulators of the Antiviral Immune Response.Viruses · 2021Review
- Transcriptomic Analysis Reveals Host miRNAs Correlated with Immune Gene Dysregulation during Fatal Disease Progression in the Ebola Virus Cynomolgus Macaque Disease Model.Microorganisms · 2021Article
- Transcriptional Analysis of Lymphoid Tissues from Infected Nonhuman Primates Reveals the Basis for Attenuation and Immunogenicity of an Ebola Virus Encoding a Mutant VP35 Protein.Journal of virology · 2021Article
- Analysis of an Ebola virus disease survivor whose host and viral markers were predictive of death indicates the effectiveness of medical countermeasures and supportive care.Genome medicine · 2021Article
- Article
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Authors and funding
11 authors.
Funding
Abstract
backgroundEbola virus is the causative agent of a severe syndrome in humans with a fatality rate that can approach 90 %. During infection, the host immune response is thought to become dysregulated, but the mechanisms through which this happens are not entirely understood. In this study, we analyze RNA sequencing data to determine the host response to Ebola virus infection in circulating immune cells.
resultsApproximately half of the 100 genes with the strongest early increases in expression were interferon-stimulated genes, such as ISG15, OAS1, IFIT2, HERC5, MX1 and DHX58. Other highly upregulated genes included cytokines CXCL11, CCL7, IL2RA, IL2R1, IL15RA, and CSF2RB, which have not been previously reported to change during Ebola virus infection. Comparing this response in two different models of exposure (intramuscular and aerosol) revealed a similar signature of infection. The strong innate response in the aerosol model was seen not only in circulating cells, but also in primary and secondary target tissues. Conversely, the innate immune response of vaccinated macaques was almost non-existent. This suggests that the innate response is a major aspect of the cellular response to Ebola virus infection in multiple tissues.
conclusionsEbola virus causes a severe infection in humans that is associated with high mortality. The host immune response to virus infection is thought to be an important aspect leading to severe pathology, but the components of this overactive response are not well characterized. Here, we analyzed how circulating immune cells respond to the virus and found that there is a strong innate response dependent on active virus replication. This finding is in stark contrast to in vitro evidence showing a suppression of innate immune signaling, and it suggests that the strong innate response we observe in infected animals may be an important contributor to pathogenesis.
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