ArticleJournal of virology2006
Resistance to alpha/beta interferon is a determinant of West Nile virus replication fitness and virulence.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 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
136 citing papers in PubMed, 198 citations in OpenAlex.
- IL-1β signaling promotes CNS-intrinsic immune control of West Nile virus infection.PLoS pathogens · 2012Trial
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- Exposure of negative-sense viral RNA in the cytoplasm initiates innate immunity to West Nile virus.Molecular cell · 2025Article
- Innate immune sensing and vaccine strategies against West Nile virus: role of Toll-like receptors and viral evasion mechanisms.Frontiers in microbiology · 2025Review
- Interferon-alpha/beta receptor deficiency enhances susceptibility to Powassan virus infection in mice.Frontiers in microbiology · 2025Article
- Multi-omics analysis of antiviral interactions of Elizabethkingia anophelis and Zika virus.Scientific reports · 2024Article
- Usutu virus and West Nile virus use a transcellular route of neuroinvasion across an in vitro model of the human blood-brain barrier.Npj viruses · 2024Article
- Exploring Zika Virus Impact on Endothelial Permeability: Insights into Transcytosis Mechanisms and Vascular Leakage.Viruses · 2024Review
- Viral Protein Accumulation of Zika Virus Variants Links with Regulation of Innate Immunity for Differential Control of Viral Replication, Spread, and Response to Interferon.Journal of virology · 2023Article
- Mechanism of Immune Evasion in Mosquito-Borne Diseases.Pathogens (Basel, Switzerland) · 2023Review
- Rescue and in vitro characterization of a divergent TBEV-Eu strain from the Netherlands.Scientific reports · 2023Article
- Insulin-mediated endothelin signaling is antiviral during West Nile virus infection.bioRxiv : the preprint server for biology · 2023Article
- Mosquito-borne flaviviruses and type I interferon: catch me if you can!Frontiers in microbiology · 2023Review
- Review
- Review
- A Possible Association Between Zika Virus Infection and CDK5RAP2 Mutation.Frontiers in genetics · 2021Article
- Article
- Yellow Fever Virus Down-Regulates mRNA Expression of SOCS1 in the Initial Phase of Infection in Human Cell Lines.Viruses · 2020Article
- Review
- Flavivirus Nonstructural Protein NS5 Dysregulates HSP90 to Broadly Inhibit JAK/STAT Signaling.Cells · 2020Article
76 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
The emergence of West Nile virus (WNV) in the Western Hemisphere is marked by the spread of pathogenic lineage I strains, which differ from typically avirulent lineage II strains. To begin to understand the virus-host interactions that may influence the phenotypic properties of divergent lineage I and II viruses, we compared the genetic, pathogenic, and alpha/beta interferon (IFN-alpha/beta)-regulatory properties of a lineage II isolate from Madagascar (MAD78) with those of a new lineage I isolate from Texas (TX02). Full genome sequence analysis revealed that MAD78 clustered, albeit distantly, with other lineage II strains, while TX02 clustered with emergent North American isolates, more specifically with other Texas strains. Compared to TX02, MAD78 replicated at low levels in cultured human cells, was highly sensitive to the antiviral actions of IFN in vitro, and demonstrated a completely avirulent phenotype in wild-type mice. In contrast to TX02 and other pathogenic forms of WNV, MAD78 was defective in its ability to disrupt IFN-induced JAK-STAT signaling, including the activation of Tyk2 and downstream phosphorylation and nuclear translocation of STAT1 and STAT2. However, replication of MAD78 was rescued in cells with a nonfunctional IFN-alpha/beta receptor (IFNAR). Consistent with this finding, the virulence of MAD78 was unmasked upon infection of mice lacking IFNAR. Thus, control of the innate host response and IFN actions is a key feature of WNV pathogenesis and replication fitness.
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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.