**6. RSV cell-to-cell spread**

Although RSV progeny virions mostly remain cell-associated, virus shedding occurs from the infected cell's surface and through cellular protrusions namely filopodia [8, 9]. RSV-induced syncytium (multinucleated cell) formation is a common feature of RSV infection in vitro. The syncytium involves the merging of infected cells with the adjacent uninfected cells, which allows the transfer of viral components from infected cells to the adjacent uninfected cells [171] (**Figure 3**). Mehedi et al., first showed that RSV uses a novel filopodia-driven cell-to-cell spread mechanism in the lung epithelial cells in vitro (**Figure 4**). It appears that RSV infection modulates cellular actin dynamics; particularly, actin-related protein 2/3 (ARP2/3) complexdriven actin polymerization contributes to lamellipodium and filopodium formation

#### **Figure 3.**

*RSV-induced syncytium (multinucleated cell) formation. A549 cells were infected with GFP-expressing RSV (RSV-GFP) at a multiplicity of infection of 1. At 48-hour post-infection, cells were fixed and imaged under an epifluorescence.*

#### **Figure 4.**

*Filopodia-driven RSV cell-to-cell spread. A549 cells were infected with RSV-WT (strain A) at a multiplicity of infection of 1. At 24-hour post-infection, cells were fixed, permeabilized, and stained for RSV F protein by using F-specific immunofluorescence (IFA) (green). F-actin was detected by rhodamine phalloidin staining (red). The image was taken under a stimulated emission depletion (STED) microscope.*

of cell motility. They showed the depletion of ARP2, a major constituent of the ARP2/3 complex resulted in a substantial reduction of RSV budding and filopodiadriven cell-to-cell spread [8, 172–174].

*Respiratory Syncytial Virus DOI: http://dx.doi.org/10.5772/intechopen.104771*
