Induction and evasion of innate antiviral responses by hepatitis C virus. - sprookjes - yvandenbroek - TriplyDB

Induction and evasion of innate antiviral responses by hepatitis C virus.

Induction and evasion of innate antiviral responses by hepatitis C virus.

http://www.wikidata.org/entity/Q34003764

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The antiviral protein viperin inhibits hepatitis C virus replication via interaction with nonstructural protein 5A Genetic variants at the IFNL3 locus and their association with hepatitis C virus infections reveal novel insights into host-virus interactions Innate immune responses in hepatitis C virus infection Collaboration of Toll-like and RIG-I-like receptors in human dendritic cells: tRIGgering antiviral innate immune responses Adenosine deaminases acting on RNA (ADARs) are both antiviral and proviral SH2 modified STAT1 induces HLA-I expression and improves IFN-γ signaling in IFN-α resistant HCV replicon cells.Direct-acting antiviral agents and the path to interferon independence.Thematic minireview series: elucidating hepatitis C virus-host interactions at the biochemical level.Disruption of TLR3 signaling due to cleavage of TRIF by the hepatitis A virus protease-polymerase processing intermediate, 3CD.An interferon response gene signature is associated with the therapeutic response of hepatitis C patients Impaired expression of type I and type II interferon receptors in HCV-associated chronic liver disease and liver cirrhosis.Canine hepacivirus NS3 serine protease can cleave the human adaptor proteins MAVS and TRIF.IFN-λ Inhibits MiR-122 Transcription through a Stat3-HNF4α Inflammatory Feedback Loop in an IFN-α Resistant HCV Cell Culture System.Class A scavenger receptor 1 (MSR1) restricts hepatitis C virus replication by mediating toll-like receptor 3 recognition of viral RNAs produced in neighboring cells.IL28B inhibits hepatitis C virus replication through the JAK-STAT pathway.Complexity and catalytic efficiency of hepatitis C virus (HCV) NS3 and NS4A protease quasispecies influence responsiveness to treatment with pegylated interferon plus ribavirin in HCV/HIV-coinfected patients Acute hepatitis A virus infection is associated with a limited type I interferon response and persistence of intrahepatic viral RNA.Differential, type I interferon-mediated autophagic trafficking of hepatitis C virus proteins in mouse liver.Protease inhibitor-resistant hepatitis C virus mutants with reduced fitness from impaired production of infectious virus Persistent Foot-and-Mouth Disease Virus Infection in the Nasopharynx of Cattle; Tissue-Specific Distribution and Local Cytokine Expression.Activation of chemokine and inflammatory cytokine response in hepatitis C virus-infected hepatocytes depends on Toll-like receptor 3 sensing of hepatitis C virus double-stranded RNA intermediates STAT1 is Constitutively Activated in the T/C28a2 Immortalized Juvenile Human Chondrocyte Line and Stimulated by IL-6 Plus Soluble IL-6R The more you look, the more you find: effects of hepatitis C virus testing interval on reinfection incidence and clearance and implications for future vaccine study design.Systematic identification of anti-interferon function on hepatitis C virus genome reveals p7 as an immune evasion protein.Emerging roles of interferon-stimulated genes in the innate immune response to hepatitis C virus infection Human type 2 myeloid dendritic cells produce interferon-λ and amplify interferon-α in response to hepatitis C virus infection.Anti-viral CD8 T cells and the cytokines that they love Elevated on-treatment levels of serum IFN-gamma is associated with treatment failure of peginterferon plus ribavirin therapy for chronic hepatitis C.Hepatitis C virus clearance, reinfection, and persistence, with insights from studies of injecting drug users: towards a vaccine Contrasting roles of mitogen-activated protein kinases in cellular entry and replication of hepatitis C virus: MKNK1 facilitates cell entry.Virus-specific mechanisms of carcinogenesis in hepatitis C virus associated liver cancer Interleukin-1 and tumor necrosis factor-α trigger restriction of hepatitis B virus infection via a cytidine deaminase activation-induced cytidine deaminase (AID)ADARs: viruses and innate immunity.HCV infection selectively impairs type I but not type III IFN signaling.Innate immune response induced by baculovirus attenuates transgene expression in mammalian cells.The effects of female sex, viral genotype, and IL28B genotype on spontaneous clearance of acute hepatitis C virus infection Viral genome imaging of hepatitis C virus to probe heterogeneous viral infection and responses to antiviral therapies.Host genetic basis for hepatitis C virus clearance: a role for blood collection centers Nonstructural protein 3-4A: the Swiss army knife of hepatitis C virus.Hepatitis C virus genotype 3: a genotype that is not 'easy-to-treat'.

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P2860

Induction and evasion of innate antiviral responses by hepatitis C virus.

http://www.wikidata.org/entity/Q34003764

description

2010 nî lūn-bûn

@nan

2010 թուականի Մայիսին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի մայիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

@zh-hk

2010年論文

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2010年論文

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2010年论文

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name

Induction and evasion of innate antiviral responses by hepatitis C virus.

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Induction and evasion of innate antiviral responses by hepatitis C virus.

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Induction and evasion of innate antiviral responses by hepatitis C virus.

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type

label

Induction and evasion of innate antiviral responses by hepatitis C virus.

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Induction and evasion of innate antiviral responses by hepatitis C virus.

@en

Induction and evasion of innate antiviral responses by hepatitis C virus.

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prefLabel

Induction and evasion of innate antiviral responses by hepatitis C virus.

@ast

Induction and evasion of innate antiviral responses by hepatitis C virus.

@en

Induction and evasion of innate antiviral responses by hepatitis C virus.

@nl

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JBC.R109.099556

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Journal of Biological Chemistry

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Induction and evasion of innate antiviral responses by hepatitis C virus.

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Stanley M Lemon

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P2860

Hepatitis C virus protease NS3/4A cleaves mitochondrial antiviral signaling protein off the mitochondria to evade innate immunity

Toll/IL-1 receptor domain-containing adaptor inducing IFN-beta (TRIF) associates with TNF receptor-associated factor 6 and TANK-binding kinase 1, and activates two distinct transcription factors, NF-kappa B and IFN-regulatory factor-3...

Interaction between the HCV NS3 protein and the host TBK1 protein leads to inhibition of cellular antiviral responses

Hepatitis C virus core protein blocks interferon signaling by interaction with the STAT1 SH2 domain

Double-stranded RNA-activated protein kinase inhibits hepatitis C virus replication but may be not essential in interferon treatment

Hepatitis C virus nonstructural protein 5A modulates the toll-like receptor-MyD88-dependent signaling pathway in macrophage cell lines

Recognition of 5' triphosphate by RIG-I helicase requires short blunt double-stranded RNA as contained in panhandle of negative-strand virus.

IPS-1, an adaptor triggering RIG-I- and Mda5-mediated type I interferon induction

Evidence that hepatitis C virus resistance to interferon is mediated through repression of the PKR protein kinase by the nonstructural 5A protein

Hepatitis C virus NS5A protein interacts with 2',5'-oligoadenylate synthetase and inhibits antiviral activity of IFN in an IFN sensitivity-determining region-independent manner

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22741-22747

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10.1074/JBC.R109.099556

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30

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285

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2010-05-10T00:00:00Z

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2906263

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