ArticleViruses2023
Nipah Virus Impairs Autocrine IFN Signaling by Sequestering STAT1 and STAT2 into Inclusion Bodies.
Article in Viruses, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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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Who cites it
15 citing papers in PubMed, 15 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
- Review
- Mpox virus D8L protein binds to STAT1 and inhibits its phosphorylation to antagonize IFN-induced signaling.Cell communication and signaling : CCS · 2026Article
- The Nipah virus threat in India: Epidemiological trends, risk drivers, and lessons for pandemic preparedness.PLoS pathogens · 2026Review
- Efficacy of the nucleoside analog 4'-Fluorouridine against Nipah virus in the Syrian hamster model.PLoS pathogens · 2026Article
- Cell-cell fusion limits activation of the unfolded protein response induced by the Nipah virus glycoproteins.Journal of virology · 2026Article
- A recombinant Cedar virus preclinical model that recapitulates neurological features of henipavirus disease.iScience · 2025Article
- The intracellular virus-host interface of henipaviruses.Journal of virology · 2025Review
- Advancements and Challenges in Addressing Zoonotic Viral Infections with Epidemic and Pandemic Threats.Viruses · 2025Review
- Functional Involvement of Signal Transducers and Activators of Transcription in the Pathogenesis of Influenza A Virus.International journal of molecular sciences · 2024Review
- Nipah virus: epidemiology, pathogenesis, treatment, and prevention.Frontiers of medicine · 2024Review
- A Comparative Assessment of the Pathogenic Potential of Newly Discovered Henipaviruses.Pathogens (Basel, Switzerland) · 2024Review
- Human Papillomavirus Carcinogenicity and the Need of New Perspectives: Thoughts from a Retrospective Analysis on Human Papillomavirus Outcomes Conducted at the Hospital University of Bari, Apulia, Italy, between 2011 and 2022.Diagnostics (Basel, Switzerland) · 2024Article
- Pathogenicity and virulence of henipaviruses.Virulence · 2023Review
- Host Cell-Virus Interaction 2.0: Viral Stratagems of Immune Evasion, Host Cellular Responses and Antiviral Counterattacks.Viruses · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nipah virus (NiV) is an emerging zoonotic paramyxovirus that causes fatal infections in humans. As with most disease-causing viruses, the pathogenic potential of NiV is linked to its ability to block antiviral responses, e.g., by antagonizing IFN signaling through blocking STAT proteins. One of the STAT1/2-binding proteins of NiV is the phosphoprotein (P), but its functional role in IFN antagonism in a full viral context is not well defined. As NiV P is required for genome replication and specifically accumulates in cytosolic inclusion bodies (IBs) of infected cells, we hypothesized that this compartmentalization might play a role in P-mediated IFN antagonism. Supporting this notion, we show here that NiV can inhibit IFN-dependent antiviral signaling via a NiV P-dependent sequestration of STAT1 and STAT2 into viral IBs. Consequently, the phosphorylation/activation and nuclear translocation of STAT proteins in response to IFN is limited, as indicated by the lack of nuclear pSTAT in NiV-infected cells. Blocking autocrine IFN signaling by sequestering STAT proteins in IBs is a not yet described mechanism by which NiV could block antiviral gene expression and provides the first evidence that cytosolic NiV IBs may play a functional role in IFN antagonism.
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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 Socratic graph.