ArticleNature communications2023
Blockade of interferon signaling decreases gut barrier integrity and promotes severe West Nile virus disease.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.
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.
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.
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Who cites it
21 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Systematic Review and Meta-analysis of Anti-interferon Auto-antibodies in Infectious Diseases.Journal of clinical immunology · 2026Pooled it
- Inflammatory Response Associated with West Nile Neuroinvasive Disease: A Systematic Review.Viruses · 2024Pooled it
- Article
- Autoantibodies neutralizing type I IFNs in 40% of patients with WNV encephalitis in seven new cohorts.Journal of human immunity · 2026Article
- Interferon-α and -β subtypes have temporally distinct roles in containing viral spread and protecting vital organs.Research square · 2026Article
- Human antibodies against West Nile and related orthoflaviviruses.bioRxiv : the preprint server for biology · 2026Article
- MyD88 signaling in myeloid cells induces gastrointestinal tract injury and systemic inflammation after West Nile virus infection.Cell reports · 2026Article
- Auto-Abs against type I IFNs: Strong, common, and global determinants of severe arboviral diseases.Journal of human immunity · 2026Review
- Detection of autoantibodies against Interferon Type I in patients with autochthonous West Nile Virus encephalitis.Brain, behavior, & immunity - health · 2025Article
- Autoantibodies neutralizing type I IFNs in 40% of patients with WNV encephalitis in seven new cohorts.medRxiv : the preprint server for health sciences · 2025Article
- Interferons in health and disease.Cell · 2025Review
- Cellular Immune Response in Horses After West Nile Neuroinvasive Disease.Animals : an open access journal from MDPI · 2025Article
- Sterile production of interferons in the thymus.Journal of immunology (Baltimore, Md. : 1950) · 2025Review
- Human inborn errors of immunity: 2024 update on the classification from the International Union of Immunological Societies Expert Committee.Journal of human immunity · 2025Article
- Human type I interferons protect Vero E6 and ARPE-19 cells against West Nile virus and are neutralized by pathogenic autoantibodies.Scientific reports · 2025Article
- West Nile Virus (WNV): One-Health and Eco-Health Global Risks.Veterinary sciences · 2025Review
- West Nile virus unmasked: from gene variability to future challenges.Frontiers in cellular and infection microbiology · 2025Review
- Article
- Loss of tolerance precedes triggering and lifelong persistence of pathogenic type I interferon autoantibodies.The Journal of experimental medicine · 2024Article
- Innate and adaptive immune responses that control lymph-borne viruses in the draining lymph node.Cellular & molecular immunology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
The determinants of severe disease caused by West Nile virus (WNV) and why only ~1% of individuals progress to encephalitis remain poorly understood. Here, we use human and mouse enteroids, and a mouse model of pathogenesis, to explore the capacity of WNV to directly infect gastrointestinal (GI) tract cells and contribute to disease severity. At baseline, WNV poorly infects human and mouse enteroid cultures and enterocytes in mice. However, when STAT1 or type I interferon (IFN) responses are absent, GI tract cells become infected, and this is associated with augmented GI tract and blood-brain barrier (BBB) permeability, accumulation of gut-derived molecules in the brain, and more severe WNV disease. The increased gut permeability requires TNF-α signaling, and is absent in WNV-infected IFN-deficient germ-free mice. To link these findings to human disease, we measured auto-antibodies against type I IFNs in serum from WNV-infected human cohorts. A greater frequency of auto- and neutralizing antibodies against IFN-α2 or IFN-ω is present in patients with severe WNV infection, whereas virtually no asymptomatic WNV-infected subjects have such antibodies (odds ratio 24 [95% confidence interval: 3.0 - 192.5; P = 0.003]). Overall, our experiments establish that blockade of type I IFN signaling extends WNV tropism to enterocytes, which correlates with increased gut and BBB permeability, and more severe disease.
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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.