Recent studies on these viruses have shown surprisingly that whereas CV-A9 uses novel HSPA5 receptor and Arf6- and dynamin-dependent entry route in infection, cellular entry of E-1 alleviates the route of the natural ligand in integrin β1; E-1 binds inactive receptor form, and internalization is dependent on clustering and not on integrin-mediated signals. Here, DNM1 is linked to infection.