Asymmetric budding of viruses in ependymal and choroid plexus epithelial cells.
Sendai virus injected intracerebrally into 3-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.
D000818:Animals; D002831:Choroid Plexus / Q000382:microbiology*; D004805:Ependyma / Q000382:microbiology*; D004848:Epithelium / Q000032:analysis / Q000382:microbiology / Q000473:pathology / Q000648:ultrastructure; D007158:Immunologic Techniques; D051379:Mice; D008815:Mice, Inbred Strains; D010222:Parainfluenza Virus 1, Human; D018184:Paramyxoviridae Infections / Q000382:microbiology*; D014759:Viral Envelope Proteins / Q000032:analysis; D014779:Virus Replication
D014759:Viral Envelope Proteins