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ASYMMETRIC BUDDING OF VIRUSES IN EPENDYMAL AND CHOROID PLEXUS EPITHELIAL CELLS
Author(s) -
KRISTENSSON K.,
LUNDH B.,
NORRBY E.,
PAYNE L.,
ÖRVELL C.
Publication year - 1984
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/j.1365-2990.1984.tb00352.x
Subject(s) - ependymal cell , budding , choroid plexus , biology , vesicular stomatitis virus , virology , sendai virus , virus , cytoplasm , viral envelope , viral replication , glycoprotein , microbiology and biotechnology , immunohistochemistry , immunology , central nervous system , neuroscience
Sendai virus injected intracerebrally into %week‐old mice caused infection of ependymal and choroid plexus epithelial cells. Budding of mature viruses occurred only from the apical surfaces of these cells. The viral peplomere proteins, haemagglutinin‐neuraminidase and fusion, were concentrated on the apical portion of the ependymal cells, while the nucleocapsid‐associated polymerase protein was dispersed throughout the cytoplasm. This indicates that intracellular routing of the virus envelope glycoproteins to the cell surface may be one of the factors that determines the site of virus budding. Vesicular stomatitis and vaccinia viruses, on the other hand, budded or egressed predominantly from the baso‐lateral cell surfaces.