Entry of hepatitis B virus: going beyond NTCP to the nucleus

Abstract

Hepatitis B virus (HBV) infection remains a major cause of liver diseases and hepatocellular carcinoma. HBV infection begins by low-affinity attachment to hepatocytes and subsequent binding with a specific receptor sodium taurocholate cotransporting polypeptide (NTCP) on sinusoidal-basolateral side of liver parenchymal cells. Following internalization with an unclear mechanism, HBV undergoes uncoating, capsid disassembling and culminates in delivering its genome into the nucleus and forms the covalently closed circular (ccc) DNA. In this review, we briefly summarize the current understanding of HBV entry and discuss some unanswered questions along the entry pathway beyond NTCP binding into the nucleus.