Epidermal growth factor receptor (EGFR) has been implicated in infection by a wide range of unrelated viruses (50), including the spread and motility of vaccinia virus (51) and the processes of endocytosis (for influenza A and HCV), and entry and/or post-entry events (for human cytomegalovirus (HCMV) and adeno-associated virus serotype A (AAV6) (Table 1) (52) (53) (54) (55) (56) (57). In fact, among the first studies to show that tyrosine kinase inhibitors can have significant antiviral activity was one identifying EGFR as a co-factor for entry of HCV into human host cells (56). EGFR is also used by different viruses, including many respiratory viruses, to evade the host immune response (58). Activity against HCMV and HCV in vitro and in vivo has been demonstrated by the EGFR-targeting inhibitors, gefitinib and erlotinib (59) (56) (57).