We also determined if similar effects on the EGF pathway were observed in infected cells. HEK-293T cells were infected with hPIV3 (MOI = 3) and then transfected with Elk1 activity reporter plasmids. Infection of HEK-293T cells was confirmed by anti-hPIV3 hemagglutinin-neuraminidase (hPIV3-HN) immunostaining and flow cytometry analysis ( Figure 2E ). Like hPIV3-C alone, hPIV3 infection enhanced Elk1 activity upon EGF stimulation ( Figure 2C ). Interestingly, hPIV3 infection induced a significant level of Elk1 activity in the absence of EGF stimulation. This suggests that in addition to hPIV3-C interaction with GRB2, other mechanisms modulate MAPK/ERK pathway during hPIV3 infection.