The superinfection exclusion of VSV has been studied and found to be caused by a combination of three distinct effects on endocytosis by VSV-infected cells: first, a decreased rate of formation of endocytic vesicles as judged by an inhibition of fluid-phase uptake at 2 hr postinfection; second, a decreased rate of internalization of receptor-bound ligands, which was detected at 4 hr postinfection; and third, a competition with newly synthesized virus for occupancy of coated pits, as indicated by electron microscopy of infected cells. At the same time that fluid-phase uptake decreased, numerous uncoated invaginations were observed at the cell surface.