In Vivo and In Vitro Models of Demyelinating Disease: A Phosphoprotein Phosphatase in Host Cell Endosomes Dephosphorylating the Nucleocapsid Protein of Coronavirus JHM
Coronavirus JHM (JHMV) shows specific tropism for oligodendrocytes of the CNS.1 Primary oligodendrocytes induced to differentiate using agents like dibutyryl cyclic AMP (dbcAMP) develop resistance to JHMV infection.1,2 Several studies suggest that the virus enters the host cell through receptor mediated endocytosis.3,4 Earlier studies also found that the nucleocapsid protein (NC) of JHMV is reduced in molecular weight (MW) from a 56K to a 50K component during the early stages of infection.5 A change in the molecular weight of this magnitude with phosphorylated proteins can be accounted for by dephosphorylation.6 The reversible phosphorylation-dephosphorylation of a capsid polypeptide-nucleic acid binding protein has been shown to influence the binding of nucleic acid in a retrovirus.7 This information suggests that a phosphoprotein phosphatase (PPPase) dephosphorylating the NC of JHMV effects the uncoating of the RNA genome during the early stages of infection. Here we present evidence for such a dephosphorylating activity in neural and other cells which are hosts for JHMV.
KeywordsDemyelinating Disease Nucleocapsid Protein Murine Fibroblast Phosphoprotein Phosphatase Coronavirus Infection
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