ArticleJournal of virology2007
West Nile virus infection activates the unfolded protein response, leading to CHOP induction and apoptosis.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers.
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Who cites it
155 citing papers in PubMed, 238 citations in OpenAlex.
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- West Nile virus and Zika virus infections induce aggresome formation in human neural progenitor and A549 cells.Journal of virology · 2026Article
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- Divergent roles of Hsp70 chaperones in orthoflavivirus protein secretion and virion formation.Npj viruses · 2026Article
- Sequelae of viral CNS infections including outcomes, mechanisms, and knowledge gaps.Npj viruses · 2025Review
- Granular Insights on Innate and Intrinsic Immunity to Flaviviruses.Microorganisms · 2025Review
- PARP-16 regulates the PERK and IRE-1α Mediated Unfolded Protein Response in Japanese Encephalitis Virus-Infected Neural Stem/Progenitor Cells.Molecular neurobiology · 2025Article
- Orf132: a critical gene for LSDV replication and its role in Er stress-related apoptosis.Virology journal · 2025Article
- Modes of action of a small molecule antiviral compound targeting yellow fever virus NS4B protein.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Role of endoplasmic reticulum stress in cell apoptosis induced by duck hepatitis A virus type 1 infection.Frontiers in immunology · 2025Article
- Genotype-Dependent Modulation of Macrophage Apoptosis and T Lymphocyte Responses by Duck Tembusu Virus Potentially Contributes to Genotype-Specific Immunopathogenesis.Transboundary and emerging diseases · 2025Article
- Activation of ATF3 via the integrated stress response pathway regulates innate immune response to restrict Zika virus.Journal of virology · 2024Article
- CD11b maintains West Nile virus replication through modulation of immune response in human neuroblastoma cells.Virology journal · 2024Article
- Activation of ATF3 via the Integrated Stress Response Pathway Regulates Innate Immune Response to Restrict Zika Virus.bioRxiv : the preprint server for biology · 2024Article
- Molecular Mechanisms Associated with Neurodegeneration of Neurotropic Viral Infection.Molecular neurobiology · 2024Review
- Apoptotic Cell Death in an Animal Model of Virus-Induced Acute Liver Failure-Observations duringInternational journal of molecular sciences · 2024Article
- An RBM10 and NF-κB interacting host lncRNA promotes JEV replication and neuronal cell death.Journal of virology · 2023Article
- Higher replication potential of West Nile virus governs apoptosis induction in human neuroblastoma cells.Apoptosis : an international journal on programmed cell death · 2023Article
- Replication of standard bovine viral diarrhea strain OregonC24Va induces endoplasmic reticulum stress-mediated apoptosis of bovine trophoblast cells.Cell stress & chaperones · 2023Article
95 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
West Nile virus (WNV)-mediated neuronal death is a hallmark of WNV meningitis and encephalitis. However, the mechanisms of WNV-induced neuronal damage are not well understood. We investigated WNV neuropathogenesis by using human neuroblastoma cells and primary rat hippocampal neurons. We observed that WNV activates multiple unfolded protein response (UPR) pathways, leading to transcriptional and translational induction of UPR target genes. We evaluated the role of the three major UPR pathways, namely, inositol-requiring enzyme 1-dependent splicing of X box binding protein 1 (XBP1) mRNA, activation of activating transcription factor 6 (ATF6), and protein kinase R-like endoplasmic reticulum (ER) kinase-dependent eukaryotic initiation factor 2alpha (eIF2alpha) phosphorylation, in WNV-infected cells. We show that XBP1 is nonessential or can be replaced by other UPR pathways in WNV replication. ATF6 was rapidly degraded by proteasomes, consistent with induction of ER stress by WNV. We further observed a transient phosphorylation of eIF2alpha and induction of the proapoptotic cyclic AMP response element-binding transcription factor homologous protein (CHOP). WNV-infected cells exhibited a number of apoptotic phenotypes, such as (i) induction of growth arrest and DNA damage-inducible gene 34, (ii) activation of caspase-3, and (iii) cleavage of poly(ADP-ribose) polymerase. The expression of WNV nonstructural proteins alone was sufficient to induce CHOP expression. Importantly, WNV grew to significantly higher viral titers in chop(-)(/)(-) mouse embryonic fibroblasts (MEFs) than in wild-type MEFs, suggesting that CHOP-dependent premature cell death represents a host defense mechanism to limit viral replication that might also be responsible for the widespread neuronal loss observed in WNV-infected neuronal tissue.
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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.