Selected article for: "capsid protein and host cell"

Author: Dales, S
Title: Factors controlling coronavirus infections and disease of the central nervous system. A review.
  • Cord-id: c888lr7y
  • Document date: 1995_1_1
  • ID: c888lr7y
    Snippet: There is a correlation between specificity of tropism of JHMV for O-2A lineage cells from the rat and demyelination of white matter, associated with chronic disease. Susceptibility to infection, which can occur in O-2A cells before terminal differentiation may be influenced by cytokines. During the normal, age-related or rapidly induced maturation/differentiation of rat oligodendrocytes, suppression of JHMV replication is correlated with upregulation of the subunit R1 of the cAMP-dependent prote
    Document: There is a correlation between specificity of tropism of JHMV for O-2A lineage cells from the rat and demyelination of white matter, associated with chronic disease. Susceptibility to infection, which can occur in O-2A cells before terminal differentiation may be influenced by cytokines. During the normal, age-related or rapidly induced maturation/differentiation of rat oligodendrocytes, suppression of JHMV replication is correlated with upregulation of the subunit R1 of the cAMP-dependent protein kinase. Virus inhibition occurs at a stage between penetration and initiation of genome expression. Regulation over coronavirus infection of oligodendroglia is strictly controlled by the host cell. There is evidence that induction of R1 subunit of protein kinase A influences uncoating, illustrated in Figure 9, by suppression of dephosphorylation during penetration. Our former working hypothesis, now borne out by recent data predicts that the infection in mature oligodendrocytes is blocked because specific dephosphorylation of the capsid protein N, required for uncoating, etc., is suppressed.

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