MyD88 is required for protection from lethal infection with a mouse-adapted SARS-CoV.
about
Molecular pathology of emerging coronavirus infectionsInflammatory monocytes and the pathogenesis of viral encephalitisEarly Upregulation of Acute Respiratory Distress Syndrome-Associated Cytokines Promotes Lethal Disease in an Aged-Mouse Model of Severe Acute Respiratory Syndrome Coronavirus InfectionA decade after SARS: strategies for controlling emerging coronavirusesThe role of epidermal growth factor receptor (EGFR) signaling in SARS coronavirus-induced pulmonary fibrosis.Interaction between innate immunity and porcine reproductive and respiratory syndrome virus.Toll-like receptors, chemokine receptors and death receptor ligands responses in SARS coronavirus infected human monocyte derived dendritic cells.Evasion by stealth: inefficient immune activation underlies poor T cell response and severe disease in SARS-CoV-infected mice.SARS-CoV pathogenesis is regulated by a STAT1 dependent but a type I, II and III interferon receptor independent mechanism.Severe acute respiratory syndrome coronavirus envelope protein ion channel activity promotes virus fitness and pathogenesisCellular immune responses to severe acute respiratory syndrome coronavirus (SARS-CoV) infection in senescent BALB/c mice: CD4+ T cells are important in control of SARS-CoV infection.Gamma interferon signaling in oligodendrocytes is critical for protection from neurotropic coronavirus infectionAllelic Variation in the Toll-Like Receptor Adaptor Protein Ticam2 Contributes to SARS-Coronavirus Pathogenesis in Mice.Immunogenicity and efficacy of a plasmid DNA rabies vaccine incorporating Myd88 as a genetic adjuvant.The PDZ-binding motif of severe acute respiratory syndrome coronavirus envelope protein is a determinant of viral pathogenesis.Effects of Toll-like receptor stimulation on eosinophilic infiltration in lungs of BALB/c mice immunized with UV-inactivated severe acute respiratory syndrome-related coronavirus vaccine.Severe acute respiratory syndrome coronavirus envelope protein regulates cell stress response and apoptosis.T cell responses are required for protection from clinical disease and for virus clearance in severe acute respiratory syndrome coronavirus-infected mice.MTA1 coregulator regulates LPS response via MyD88-dependent signalingCoronavirus papain-like proteases negatively regulate antiviral innate immune response through disruption of STING-mediated signalingTranscriptomic analysis reveals a mechanism for a prefibrotic phenotype in STAT1 knockout mice during severe acute respiratory syndrome coronavirus infection.Toll-like receptor 4-mediated activation of p38 mitogen-activated protein kinase is a determinant of respiratory virus entry and tropismMyD88 signaling is indispensable for primary influenza A virus infection but dispensable for secondary infectionSuccessful vaccination strategies that protect aged mice from lethal challenge from influenza virus and heterologous severe acute respiratory syndrome coronavirus.Coronavirus non-structural protein 16: evasion, attenuation, and possible treatments.Delivery route, MyD88 signaling and cross-priming events determine the anti-tumor efficacy of an adenovirus based melanoma vaccine.Kaposi's sarcoma-associated herpesvirus-encoded replication and transcription activator impairs innate immunity via ubiquitin-mediated degradation of myeloid differentiation factor 88Epithelial cells lining salivary gland ducts are early target cells of severe acute respiratory syndrome coronavirus infection in the upper respiratory tracts of rhesus macaques.Toll-Like Receptor 3 Signaling via TRIF Contributes to a Protective Innate Immune Response to Severe Acute Respiratory Syndrome Coronavirus InfectionMolecular determinants of severe acute respiratory syndrome coronavirus pathogenesis and virulence in young and aged mouse models of human disease.Genome Wide Identification of SARS-CoV Susceptibility Loci Using the Collaborative Cross.The effect of inhibition of PP1 and TNFα signaling on pathogenesis of SARS coronavirusBoth Cerebral and Hematopoietic Deficiencies in CCR2 Result in Uncontrolled Herpes Simplex Virus Infection of the Central Nervous System in Mice.Identification of the Mechanisms Causing Reversion to Virulence in an Attenuated SARS-CoV for the Design of a Genetically Stable Vaccine.A live, impaired-fidelity coronavirus vaccine protects in an aged, immunocompromised mouse model of lethal disease.Mechanisms of severe acute respiratory syndrome coronavirus-induced acute lung injury.Experimental and natural infections in MyD88- and IRAK-4-deficient mice and humansWild-type and innate immune-deficient mice are not susceptible to the Middle East respiratory syndrome coronavirus.Epigenetic Landscape during Coronavirus InfectionThe role of toll-like receptors in acute and chronic lung inflammation.
P2860
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P2860
MyD88 is required for protection from lethal infection with a mouse-adapted SARS-CoV.
description
2008 nî lūn-bûn
@nan
2008 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2008 թվականի դեկտեմբերին հրատարակված գիտական հոդված
@hy
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
name
MyD88 is required for protection from lethal infection with a mouse-adapted SARS-CoV.
@ast
MyD88 is required for protection from lethal infection with a mouse-adapted SARS-CoV.
@en
type
label
MyD88 is required for protection from lethal infection with a mouse-adapted SARS-CoV.
@ast
MyD88 is required for protection from lethal infection with a mouse-adapted SARS-CoV.
@en
prefLabel
MyD88 is required for protection from lethal infection with a mouse-adapted SARS-CoV.
@ast
MyD88 is required for protection from lethal infection with a mouse-adapted SARS-CoV.
@en
P2093
P2860
P1433
P1476
MyD88 is required for protection from lethal infection with a mouse-adapted SARS-CoV.
@en
P2093
Satoshi Uematsu
Shizou Akira
Thomas E Morrison
Timothy Sheahan
William Funkhouser
P2860
P304
P356
10.1371/JOURNAL.PPAT.1000240
P577
2008-12-12T00:00:00Z