Altogether, these data demonstrate that hPIV3 infection or hPIV3-C expression alone both enhance MAPK/ERK pathway activation in EGF-stimulated cells. Several RNA viruses require an activated MAPK/ERK pathway to produce viral components and replicate properly (for review see [31] ). To test if the same was true for hPIV3, cells were treated for 2 h with MAPK/ERK pathway inhibitor U0126 and infected with hPIV3 (MOI = 1). Two days after infection, cell surface expression of hPIV3-HN was detected by immunostaining and flow cytometry. U0126 completely blocked the expression of hPIV3-HN in hPIV3-infected cells (Figure 4 ), whereas the same inhibitor had no effect when cells were infected with MV ( Figure S2 ). Altogether, this demonstrates that MAPK/ERK signaling is essential for the expression of hPIV3 proteins and suggests that hPIV3 manipulates this pathway to increase replication efficiency.