ArticleScientific reports2016
Identification of host genes leading to West Nile virus encephalitis in mice brain using RNA-seq analysis.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Inflammatory Response Associated with West Nile Neuroinvasive Disease: A Systematic Review.Viruses · 2024Pooled it
- Nangibotide in patients with septic shock: a Phase 2a randomized controlled clinical trial.Intensive care medicine · 2020Trial
- NLRC5 restricts Japanese encephalitis virus replication and neuroinflammation by interacting with the viral NS3 protein in an IFN-γ-dependent manner.Journal of neuroinflammation · 2026Article
- Transcriptomic insights into the neuropathogenic and immune response alterations in mouse neurons challenged with west nile and japanese encephalitis viruses.Virology journal · 2026Article
- Characterization of virus neuroinvasion, blood-brain barrier integrity and neuroinflammation following Powassan virus infection in mice.Frontiers in immunology · 2026Article
- TREM-1 Interacts with Rotavirus Proteins and Drives Inflammatory Responses: A Combined Experimental and Computational Approach.Pathogens (Basel, Switzerland) · 2025Article
- Article
- Effects of West Nile virus on behavioral and cognitive performance, cortical Aβ pathology, viral loads, and immune measures of middle-aged NL-G-F/E3 and NL-G-F/E4 mice.Frontiers in aging neuroscience · 2025Article
- Virus-specific host responses and gene signatures following infection with major SARS-CoV-2 variants of concern: role of ZBP1 in viral clearance and lung inflammation.Frontiers in immunology · 2025Article
- Upregulation of Neuroinflammation-Associated Genes in the Brain of SARS-CoV-2-Infected Mice.Pathogens (Basel, Switzerland) · 2024Article
- Article
- Classical swine fever virus non-structural protein 5B hijacks host METTL14-mediated m6A modification to counteract host antiviral immune response.PLoS pathogens · 2024Article
- Interleukins, Chemokines, and Tumor Necrosis Factor Superfamily Ligands in the Pathogenesis of West Nile Virus Infection.Viruses · 2023Review
- ZBP1: A Powerful Innate Immune Sensor and Double-Edged Sword in Host Immunity.International journal of molecular sciences · 2022Review
- Intrinsic antiviral immunity of barrier cells revealed by an iPSC-derived blood-brain barrier cellular model.Cell reports · 2022Article
- West Nile Virus Neuroinfection in Humans: Peripheral Biomarkers of Neuroinflammation and Neuronal Damage.Viruses · 2022Article
- SARS-CoV-2 Infects Primary Neurons from Human ACE2 Expressing Mice and Upregulates Genes Involved in the Inflammatory and Necroptotic Pathways.Pathogens (Basel, Switzerland) · 2022Article
- Review
- Article
- NLRC5: A Potential Target for Central Nervous System Disorders.Frontiers in immunology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Differential host responses may be critical determinants of distinct pathologies of West Nile virus (WNV) NY99 (pathogenic) and WNV Eg101 (non-pathogenic) strains. We employed RNA-seq technology to analyze global differential gene expression in WNV-infected mice brain and to identify the host cellular factors leading to lethal encephalitis. We identified 1,400 and 278 transcripts, which were differentially expressed after WNV NY99 and WNV Eg101 infections, respectively, and 147 genes were common to infection with both the viruses. Genes that were up-regulated in infection with both the viruses were mainly associated with interferon signaling. Genes associated with inflammation and cell death/apoptosis were only expressed after WNV NY99 infection. We demonstrate that differences in the activation of key pattern recognition receptors resulted in the induction of unique innate immune profiles, which corresponded with the induction of interferon and inflammatory responses. Pathway analysis of differentially expressed genes indicated that after WNV NY99 infection, TREM-1 mediated activation of toll-like receptors leads to the high inflammatory response. In conclusion, we have identified both common and specific responses to WNV NY99 and WNV Eg101 infections as well as genes linked to potential resistance to infection that may be targets for therapeutics.
Indexed as
Identifiers
What OpenQuestion holds
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.