We hypothesize that induction of virus-containing filopodia could be important for SARS-CoV-2 egress and/or cell-to-cell spread within epithelial monolayers. Given that Rho/PAK/ROCK signaling is downregulated, we next asked whether CK2 could play a role in this process. At 24 h, infected cells showed CK2 expression along the thin filopodial protrusions (Figure 5E), partially co-localized with SARS-CoV-2 N protein (Figure 5F). Scanning and transmission electron microscopy were used (Figures 5G, 5H, S3C, and S3D) to image the cellular protrusions at higher resolution. Assembled viral particles are clearly visible along these filopodia (Figure 5G), with instances where the viral particles appear to be budding from the protrusions (Figure 5H). Finally, we performed a global phosphoproteomics analysis of Vero E6 cells overexpressing N protein and observed CK2 activity to be significantly upregulated (Figure S3E; Tables S1 and S4). Because CK2 activity can promote actin polymerization (D’Amore et al., 2019), we hypothesize that N protein may allosterically control CK2 activity and regulate cytoskeleton organization.