NTCP ubiquitination enables HBV infection

This study contributes to elucidating the process of how HBV enters hepatocytes, which is largely elusive. NTCP was found not only to be required for the binding of HBV to hepatocytes, but also to have a crucial role in hepatic internalization of HBV. In addition, a K at position 340 was identified as the main ubiquitination target of NTCP; ubiquitination-mediated endocytosis of NTCP at this position is likely to be the mechanism regulating HBV internalization. Thus, interfering with NTCP ubiquitination could provide a novel means to reduce HBV infection.