ArticleViral immunology2011
West Nile virus infection induces depletion of IFNAR1 protein levels.
Article in Viral immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
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
26 citing papers in PubMed, 41 citations in OpenAlex.
- Interplay between flaviviruses and the interferon response: mechanisms of immune evasion and therapeutic implications.Frontiers in pharmacology · 2026Review
- PIM1 Attenuates Innate Immunity to Foster Coronavirus Replication through Ubiquitin Ligase β-TrCP-Mediated IFNAR1 Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Flavivirus Non-Structural Protein 5 (NS5): Structure, Functions, and Targeting for Development of Vaccines and Therapeutics.Vaccines · 2024Review
- Mechanism of Immune Evasion in Mosquito-Borne Diseases.Pathogens (Basel, Switzerland) · 2023Review
- Mosquito-borne flaviviruses and type I interferon: catch me if you can!Frontiers in microbiology · 2023Review
- Targeting Type I Interferon Induction and Signaling: How Zika Virus Escapes from Host Innate Immunity.International journal of biological sciences · 2023Review
- Pathogenicity and virulence of West Nile virus revisited eight decades after its first isolation.Virulence · 2021Article
- Feline calicivirus strain 2280 p30 antagonizes type I interferon-mediated antiviral innate immunity through directly degrading IFNAR1 mRNA.PLoS pathogens · 2020Article
- Review
- STAT5: a Target of Antagonism by Neurotropic Flaviviruses.Journal of virology · 2019Article
- The potential contribution of impaired brain glucose metabolism to congenital Zika syndrome.Journal of anatomy · 2019Review
- Article
- Viral Encephalitis and Neurologic Diseases: Focus on Astrocytes.Trends in molecular medicine · 2018Review
- Review
- Investigation of sphingosine kinase 1 in interferon responses during dengue virus infection.Clinical & translational immunology · 2017Article
- The Many Faces of the Flavivirus NS5 Protein in Antagonism of Type I Interferon Signaling.Journal of virology · 2017Review
- Innate immune escape by Dengue and West Nile viruses.Current opinion in virology · 2016Review
- Flavivirus Antagonism of Type I Interferon Signaling Reveals Prolidase as a Regulator of IFNAR1 Surface Expression.Cell host & microbe · 2015Article
- The ER quality control and ER associated degradation machineries are vital for viral pathogenesis.Frontiers in plant science · 2014Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Productive virus infection requires evasion, inhibition, or subversion of innate immune responses. West Nile virus (WNV), a human pathogen that can cause symptomatic infections associated with meningitis and encephalitis, inhibits the interferon (IFN) signal transduction pathway by preventing phosphorylation of Janus kinases and STAT transcription factors. Inhibition of the IFN signal cascade abrogates activation of IFN-induced genes, thus attenuating an antiviral response. We investigated the mechanism responsible for this inhibition and found that WNV infection prevents accumulation of the IFN-α receptor subunit 1 (IFNAR1). The WNV-induced depletion of IFNAR1 was conserved across multiple cell types. Our results indicated that expression of WNV nonstructural proteins resulted in activated lysosomal and proteasomal protein degradation pathways independent of the unfolded protein response (UPR). Furthermore, WNV infection did not induce serine phosphorylation, a modification on IFNAR1 that precedes its natural turnover. These data demonstrate that WNV infection results in a reduction of IFNAR1 protein through a non-canonical protein degradation pathway, and may participate in the inhibition of the IFN response.
Indexed as
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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.