ArticleJournal of virology2012
Nonstructural Nipah virus C protein regulates both the early host proinflammatory response and viral virulence.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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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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
43 citing papers in PubMed, 74 citations in OpenAlex.
- Natural History of Nipah Virus in Hamsters: Strain, Route, and Sex-Associated Variability Characterized Using Large Datasets to Inform Pre-Clinical Study Design.The Journal of infectious diseases · 2026Article
- The intracellular virus-host interface of henipaviruses.Journal of virology · 2025Review
- Mechanistic insights into Nipah virus 5' UTR functionality reveal an antiviral target.The Journal of general virology · 2025Article
- Design and Preliminary Immunogenicity Evaluation of Nipah Virus Glycoprotein G Epitope-Based Peptide Vaccine in Mice.Vaccines · 2025Article
- Henipaviruses: epidemiology, ecology, disease, and the development of vaccines and therapeutics.Clinical microbiology reviews · 2025Review
- An Updated Review on Nipah Virus Infection with a Focus on Encephalitis, Vasculitis, and Therapeutic Approaches.Current topics in medicinal chemistry · 2025Review
- A Comparative Assessment of the Pathogenic Potential of Newly Discovered Henipaviruses.Pathogens (Basel, Switzerland) · 2024Review
- Pathogenicity and virulence of henipaviruses.Virulence · 2023Review
- Aggregated Hendra virus C-protein activates the NLRP3 inflammasome to induce inflammation.Journal of inflammation (London, England) · 2023Article
- Animal Models for Henipavirus Research.Viruses · 2023Review
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- Henipavirus Immune Evasion and Pathogenesis Mechanisms: Lessons Learnt from Natural Infection and Animal Models.Viruses · 2022Review
- C Proteins: Controllers of Orderly Paramyxovirus Replication and of the Innate Immune Response.Viruses · 2022Review
- Nipah virus W protein harnesses nuclear 14-3-3 to inhibit NF-κB-induced proinflammatory response.Communications biology · 2021Article
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- Evolutionary history of cotranscriptional editing in the paramyxoviral phosphoprotein gene.Virus evolution · 2021Review
- Newcastle disease virus RNA-induced IL-1β expression via the NLRP3/caspase-1 inflammasome.Veterinary research · 2020Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nipah virus (NiV) is a highly pathogenic, negative-strand RNA paramyxovirus that has recently emerged from flying foxes to cause serious human disease. We have analyzed the role of the nonstructural NiV C protein in viral immunopathogenesis using recombinant virus lacking the expression of NiV C (NiVΔC). While wild-type NiV was highly pathogenic in the hamster animal model, NiVΔC was strongly attenuated. Replication of NiVΔC was followed by the production of NiV-specific antibodies and associated with higher recruitment of inflammatory cells and less intensive histopathological lesions in different organs than in wild-type-NiV-infected animals. To analyze the molecular basis of NiVΔC attenuation, we studied early changes in gene expression in infected primary human endothelial cells, a major cellular target of NiV infection. The transcriptomic approach revealed the striking difference between wild-type and mutant NiV in the expression of genes involved in immunity, with the particularly interesting differential patterns of proinflammatory cytokines. Compared to wild-type virus, NiVΔC induced increased expression of interleukin 1 beta (IL-1β), IL-8, CXCL2, CXCL3, CXCL6, CCL20, and beta interferon. Furthermore, the expression of NiV C in stably transfected cells decreased the production of the same panel of cytokines, revealing a role of the C protein in the regulation of cytokine balance. Together, these results suggest that NiV C regulates expression of proinflammatory cytokines, therefore providing a signal responsible for the coordination of leukocyte recruitment and the chemokine-induced immune response and controlling the lethal outcome of the infection.
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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.