Tick-borne encephalitis virus delays interferon induction and hides its double-stranded RNA in intracellular membrane vesicles.
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Targeting membrane-bound viral RNA synthesis reveals potent inhibition of diverse coronaviruses including the middle East respiratory syndrome virusThe role of viral persistence in flavivirus biologyA three-dimensional comparison of tick-borne flavivirus infection in mammalian and tick cell linesHuman Tick-Borne Encephalitis and Characterization of Virus from Biting TickEndoplasmic Reticulum: The Favorite Intracellular Niche for Viral Replication and AssemblyMembranous replication factories induced by plus-strand RNA virusesTick-borne encephalitis virus induces chemokine RANTES expression via activation of IRF-3 pathwayThe many faces of the flavivirus NS5 protein in antagonism of type I interferon signalingFast type I interferon response protects astrocytes from flavivirus infection and virus-induced cytopathic effectsViperin is an iron-sulfur protein that inhibits genome synthesis of tick-borne encephalitis virus via radical SAM domain activityUltrastructural Characterization of Zika Virus Replication FactoriesThe IMPORTance of the Nucleus during Flavivirus Replication.Three-dimensional architecture of tick-borne encephalitis virus replication sites and trafficking of the replicated RNA.Electron Tomography Analysis of Tick-Borne Encephalitis Virus Infection in Human NeuronsThe stress granule component TIA-1 binds tick-borne encephalitis virus RNA and is recruited to perinuclear sites of viral replication to inhibit viral translation.Interferon regulatory factor-1 protects from fatal neurotropic infection with vesicular stomatitis virus by specific inhibition of viral replication in neuronsTRIM79α, an interferon-stimulated gene product, restricts tick-borne encephalitis virus replication by degrading the viral RNA polymeraseComparison of attenuated and virulent West Nile virus strains in human monocyte-derived dendritic cells as a model of initial human infection.Molecular Mechanisms of Interaction Between Human Immune Cells and Far Eastern Tick-Borne Encephalitis Virus StrainsWest nile virus infections suppress early viral RNA synthesis and avoid inducing the cell stress granule response.High-Throughput Screening Using a Whole-Cell Virus Replication Reporter Gene Assay to Identify Inhibitory Compounds against Rift Valley Fever Virus Infection.The Hepatitis C Virus-Induced Membranous Web and Associated Nuclear Transport Machinery Limit Access of Pattern Recognition Receptors to Viral Replication SitesType I Interferon response in olfactory bulb, the site of tick-borne flavivirus accumulation, is primarily regulated by IPS-1.Mutations in Encephalomyocarditis Virus 3A Protein Uncouple the Dependency of Genome Replication on Host Factors Phosphatidylinositol 4-Kinase IIIα and Oxysterol-Binding ProteinCell-type-specific activation of the oligoadenylate synthetase-RNase L pathway by a murine coronavirus.Lethal Experimental Tick-Borne Encephalitis Infection: Influence of Two Strains with Similar Virulence on the Immune Response.The double-stranded transcriptome of Escherichia coliSensing microbial RNA in the cytosol.Virulence factor NSs of rift valley fever virus recruits the F-box protein FBXO3 to degrade subunit p62 of general transcription factor TFIIHHepatitis C virus and host cell nuclear transport machinery: a clandestine affair.Analysis of tick-borne encephalitis virus-induced host responses in human cells of neuronal origin and interferon-mediated protection.Interferon signaling in Peromyscus leucopus confers a potent and specific restriction to vector-borne flaviviruses.Illuminating the Sites of Enterovirus Replication in Living Cells by Using a Split-GFP-Tagged Viral Protein.Delayed cytosolic exposure of Japanese encephalitis virus double-stranded RNA impedes interferon activation and enhances viral dissemination in porcine cells.Lipid Tales of Viral Replication and Transmission.The role of the poly(A) tract in the replication and virulence of tick-borne encephalitis virus.Human cell tropism and innate immune system interactions of human respiratory coronavirus EMC compared to those of severe acute respiratory syndrome coronavirus.Antagonism of type I interferon by flaviviruses.The dengue virus conceals double-stranded RNA in the intracellular membrane to escape from an interferon response.Type I interferon protects mice from fatal neurotropic infection with Langat virus by systemic and local antiviral responses.
P2860
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P2860
Tick-borne encephalitis virus delays interferon induction and hides its double-stranded RNA in intracellular membrane vesicles.
description
2010 nî lūn-bûn
@nan
2010 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի հունիսին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
name
Tick-borne encephalitis virus ...... tracellular membrane vesicles.
@ast
Tick-borne encephalitis virus ...... tracellular membrane vesicles.
@en
Tick-borne encephalitis virus ...... tracellular membrane vesicles.
@nl
type
label
Tick-borne encephalitis virus ...... tracellular membrane vesicles.
@ast
Tick-borne encephalitis virus ...... tracellular membrane vesicles.
@en
Tick-borne encephalitis virus ...... tracellular membrane vesicles.
@nl
prefLabel
Tick-borne encephalitis virus ...... tracellular membrane vesicles.
@ast
Tick-borne encephalitis virus ...... tracellular membrane vesicles.
@en
Tick-borne encephalitis virus ...... tracellular membrane vesicles.
@nl
P2860
P356
P1433
P1476
Tick-borne encephalitis virus ...... tracellular membrane vesicles.
@en
P2093
Anna K Overby
Vsevolod L Popov
P2860
P304
P356
10.1128/JVI.00176-10
P407
P577
2010-06-16T00:00:00Z