Suppression of EGFR ubiquitination by site-directed mutagenesis or by knocking down two EGFR-sorting molecules, signal-transducing adaptor molecule (STAM) and lysosomal protein transmembrane 4 β (LAPTM4B), suggested that EGFR transport to the late endosome is critical for efficient HBV infection.
By displaying affibody (Z<sub>EGFR</sub>) binding to EGFR on the surface of a bio-nanocapsule (BNC) derived from a hepatitis B virus (HBV), we developed an altered BNC (Z<sub>EGFR</sub>-BNC) with a high specificity to EGFR-expressing cells.