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Asymmetric budding of viruses in ependymal and choroid plexus epithelial cells
Abstract:
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.
Insights
Sendai virus infects brain cells, budding from apical surfaces. Viral protein location suggests cell surface routing dictates budding site, unlike other viruses.
Area of Science:
- Virology
- Cell Biology
- Neuroscience
Background:
- Understanding viral budding and cell tropism is crucial for antiviral strategies.
- The specific mechanisms determining polarized viral budding from epithelial cells remain incompletely understood.
Purpose of the Study:
- To investigate the cellular site of Sendai virus (SeV) budding in the mouse brain.
- To determine the localization of viral proteins and their role in polarized budding.
Main Methods:
- Intracerebral injection of Sendai virus into 3-week-old mice.
- Microscopic examination of infected ependymal and choroid plexus epithelial cells.
- Immunolocalization of viral proteins (haemagglutinin-neuraminidase, fusion, polymerase).
Main Results:
- Sendai virus infected ependymal and choroid plexus epithelial cells.
- Mature virus particles budded exclusively from the apical surfaces of these cells.
- Viral envelope proteins (haemagglutinin-neuraminidase, fusion) localized apically, while polymerase was cytoplasmic.
Conclusions:
- Intracellular routing of viral envelope glycoproteins to the apical cell surface dictates Sendai virus budding site.
- This apical budding contrasts with the basolateral budding observed for vesicular stomatitis and vaccinia viruses.
- Findings provide insights into the mechanisms of polarized viral morphogenesis in epithelial cells.