Abstract
Inside cells, viruses build specialized compartments for replication and morphogenesis. We observed that virus release associates with specific structures found on the surface of mammalian cells. Cultured adherent cells were infected with a bunyavirus and processed for oriented sectioning and transmission electron microscopy. Imaging of cell basal regions showed sophisticated multilamellar structures (MLS) and extracellular filament bundles with attached viruses. Correlative light and electron microscopy confirmed that both MLS and filaments proliferated during the maximum egress of new viruses. MLS dimensions and structure were reminiscent of those reported for the nanostructures on gecko fingertips, which are responsible for the extraordinary attachment capacity of these lizards. As infected cells with MLS were more resistant to detachment than control cells, we propose an adhesive function for these structures, which would compensate for the loss of adherence during release of new virus progeny.
Highlights
Viruses manipulate cell organization by recruiting materials to build scaffolds, where they replicate their genomes, assemble new infectious particles, and conceal themselves from antiviral defense sentinels of the cell [1],[2]
We previously reported that Bunyamwera virus (BUNV), the best characterized member of the family Bunyaviridae, transforms cell structure to build an intracellular factory that changes according to virus needs during the phases of genome replication and morphogenesis [22]
correlative light and electron microscopy (CLEM) and transmission electron microscopy (TEM) of control and bunyavirus-infected cells BHK-21 cells were infected with BUNV at a multiplicity of infection (M.O.I.) of 1 plaque-forming unit (PFU) per cell, and live cells were studied by video microscopy (Figure 1)
Summary
Viruses manipulate cell organization by recruiting materials to build scaffolds, where they replicate their genomes, assemble new infectious particles, and conceal themselves from antiviral defense sentinels of the cell [1],[2] These virus activities damage the cell, which can respond with self-defensive structural solutions such as specialized cytosolic or nuclear bodies in which viral factors are trapped and immobilized [3],[4]. CLEM allows pre-selection of individual live cells with features of interest, for detailed ultrastructural study in transmission electron microscopy (TEM) With these powerful tools, we can analyze complex events in heterogeneous cell populations and address the biogenesis and evolution of cell structures such as those induced by virus infection [1], [21]
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