EGFR and Reoviridae infectious disease: Interestingly, cell lines naturally resistant to reovirus infection demonstrated enhanced susceptibility when transformed with the v-erbB oncogene, which encodes for a truncated form of the EGFR lacking the extracellular ligand-binding domain but possessing constitutive tyrosine kinase activity, suggesting that reovirus infection is facilitated by EGFR-mediated pathways rather than binding of the virus to EGFR itself (27).