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Updated: Oct 23, 2025

A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target
Published on: May 10, 2022
Entry of hepatitis B virus: going beyond NTCP to the nucleus
Ji Tian1, Cong Li1, Wenhui Li1
1National Institute of Biological Science, Beijing, 7 Science Park Road, Zhongguancun Life Science Park, Beijing, 102206, China; Tsinghua Institute of Multidisciplinary Biomedical Research, Tsinghua University, Beijing, 102206, China.
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.
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