Papillomaviruses infect skin and mucosa where they induce warts and cancers. For entry to occur, they sequentially engage numerous host proteins, allowing them to deliver their genetic information into target cells. This multistep process starts with initial binding via its L1 major capsid protein, followed by structural changes of the capsid on the cell surface, engagement of different receptors, and endocytosis. The post-entry phase includes capsid disassembly, endosomal escape of a complex of the minor capsid protein L2 and the viral genome, its transport into the nucleus, and accumulation at nuclear substructures. This review summarizes the current knowledge of the papillomavirus entry pathway and the role of cellular proteins involved in this course of events.