Previous studies have shown that the human papillomavirus type 16 (HPV-16) L2 capsid protein plays an essential role in viral infection, in part through its interaction with sorting nexin 17 (SNX17). We now show that this interaction between L2 and SNX17 is conserved across multiple PV types. Furthermore, we demonstrate that SNX17 is essential for infection with all PV types analyzed, indicating an evolutionarily highly conserved virus entry mechanism.