Pathogenesis of chimeric MHV4/MHV-A59 recombinant viruses: the murine coronavirus spike protein is a major determinant of neurovirulence.
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Acquisition of macrophage tropism during the pathogenesis of feline infectious peritonitis is determined by mutations in the feline coronavirus spike proteinCharacterization of an essential RNA secondary structure in the 3' untranslated region of the murine coronavirus genomeMurine Coronavirus Mouse Hepatitis Virus Is Recognized by MDA5 and Induces Type I Interferon in Brain Macrophages/MicrogliaDemyelination determinants map to the spike glycoprotein gene of coronavirus mouse hepatitis virusIdentification of NCAM that interacts with the PHE-CoV spike protein.Retargeting of coronavirus by substitution of the spike glycoprotein ectodomain: crossing the host cell species barrierMurine coronavirus evolution in vivo: functional compensation of a detrimental amino acid substitution in the receptor binding domain of the spike glycoprotein.Murine coronavirus spike protein determines the ability of the virus to replicate in the liver and cause hepatitis.Contributions of the viral genetic background and a single amino acid substitution in an immunodominant CD8+ T-cell epitope to murine coronavirus neurovirulence.A mechanism of virus-induced demyelination.Pathogenesis of murine coronavirus in the central nervous system.Genetic determinants of mouse hepatitis virus strain 1 pneumovirulence.Murine coronavirus receptors are differentially expressed in the central nervous system and play virus strain-dependent roles in neuronal spreadCoronavirus pathogenesis and the emerging pathogen severe acute respiratory syndrome coronavirus.Palmitoylations on murine coronavirus spike proteins are essential for virion assembly and infectivity.Genetic evidence for a structural interaction between the carboxy termini of the membrane and nucleocapsid proteins of mouse hepatitis virus.Mouse hepatitis virus infection upregulates genes involved in innate immune responses.Deficient incorporation of spike protein into virions contributes to the lack of infectivity following establishment of a persistent, non-productive infection in oligodendroglial cell culture by murine coronavirus.Both spike and background genes contribute to murine coronavirus neurovirulenceSwitching species tropism: an effective way to manipulate the feline coronavirus genome.Murine coronavirus-induced hepatitis: JHM genetic background eliminates A59 spike-determined hepatotropismExpression of the mouse hepatitis virus receptor by central nervous system microgliaCell-type-specific type I interferon antagonism influences organ tropism of murine coronavirusCoronavirus cell entry occurs through the endo-/lysosomal pathway in a proteolysis-dependent manner.Effects of an epitope-specific CD8+ T-cell response on murine coronavirus central nervous system disease: protection from virus replication and antigen spread and selection of epitope escape mutants.A hypervariable region within the 3' cis-acting element of the murine coronavirus genome is nonessential for RNA synthesis but affects pathogenesisCleavage of a Neuroinvasive Human Respiratory Virus Spike Glycoprotein by Proprotein Convertases Modulates Neurovirulence and Virus Spread within the Central Nervous SystemInhibition of the alpha/beta interferon response by mouse hepatitis virus at multiple levels.The spike glycoprotein of murine coronavirus MHV-JHM mediates receptor-independent infection and spread in the central nervous systems of Ceacam1a-/- MiceAnimal origins of the severe acute respiratory syndrome coronavirus: insight from ACE2-S-protein interactions.Chimeric coronavirus-like particles carrying severe acute respiratory syndrome coronavirus (SCoV) S protein protect mice against challenge with SCoVEnhanced virulence mediated by the murine coronavirus, mouse hepatitis virus strain JHM, is associated with a glycine at residue 310 of the spike glycoprotein.Demyelinating and nondemyelinating strains of mouse hepatitis virus differ in their neural cell tropismPriming of CD8+ T cells during central nervous system infection with a murine coronavirus is strain dependent.Coronavirus neurovirulence correlates with the ability of the virus to induce proinflammatory cytokine signals from astrocytes and microglia.The spike protein of murine coronavirus regulates viral genome transport from the cell surface to the endoplasmic reticulum during infection.Immunological characterization of the spike protein of the severe acute respiratory syndrome coronavirus.Genetic analysis of determinants for spike glycoprotein assembly into murine coronavirus virions: distinct roles for charge-rich and cysteine-rich regions of the endodomain.Ifit2 deficiency results in uncontrolled neurotropic coronavirus replication and enhanced encephalitis via impaired alpha/beta interferon induction in macrophages.Murine coronavirus neuropathogenesis: determinants of virulence.
P2860
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P2860
Pathogenesis of chimeric MHV4/MHV-A59 recombinant viruses: the murine coronavirus spike protein is a major determinant of neurovirulence.
description
1999 nî lūn-bûn
@nan
1999 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
1999 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
name
Pathogenesis of chimeric MHV4/ ...... determinant of neurovirulence.
@ast
Pathogenesis of chimeric MHV4/ ...... determinant of neurovirulence.
@en
type
label
Pathogenesis of chimeric MHV4/ ...... determinant of neurovirulence.
@ast
Pathogenesis of chimeric MHV4/ ...... determinant of neurovirulence.
@en
prefLabel
Pathogenesis of chimeric MHV4/ ...... determinant of neurovirulence.
@ast
Pathogenesis of chimeric MHV4/ ...... determinant of neurovirulence.
@en
P2093
P2860
P1433
P1476
Pathogenesis of chimeric MHV4/ ...... determinant of neurovirulence.
@en
P2093
P2860
P304
P577
1999-09-01T00:00:00Z