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Related Experiment Video

Updated: Jan 8, 2026

A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target

A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target

Published on: May 10, 2022

CD46 regulates hepatitis B virus entry by modulating cell-surface NTCP levels through cis-interaction.

Kei Miyakawa^1,2,3,4, Yusuke Nakai², Taichi Kameya^5,6

¹AIDS Research Center, National Institute of Infectious Diseases, Japan Institute for Health Security, Tokyo 208-0011, Japan.

Journal of Molecular Cell Biology

|December 23, 2025

Summary

This summary is machine-generated.

CD46 regulates Hepatitis B virus (HBV) entry by controlling the expression of its receptor, sodium taurocholate co-transporting polypeptide (NTCP). Targeting CD46 with antibodies inhibits HBV infection.

Keywords:

hepatitis B virus (HBV)proximity-based labeling sodium taurocholate co-transporting polypeptide (NTCP)viral entry

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Area of Science:

Hepatology
Virology
Immunology

Background:

Hepatitis B virus (HBV) infection is a significant global health issue.
Sodium taurocholate co-transporting polypeptide (NTCP) is the main receptor for HBV entry, but its regulation is not fully understood.

Purpose of the Study:

To identify regulatory factors of NTCP-mediated HBV entry.
To investigate the role of CD46 in HBV infection.

Main Methods:

Proximity-based labeling screening to identify protein interactions.
Depletion of CD46 to assess its effect on NTCP levels and HBV infection.
Treatment with anti-CD46 monoclonal antibodies to evaluate antiviral effects.
Experiments conducted in hepatocytes and primary human hepatocytes.

Main Results:

CD46 was identified as a crucial regulator of NTCP membrane expression, interacting with NTCP in cis.
CD46 depletion reduced cell-surface NTCP and HBV infection.
Anti-CD46 antibodies inhibited HBV infection by inducing NTCP internalization.
Antiviral effects were confirmed in primary human hepatocytes.

Conclusions:

CD46 plays a key role in regulating NTCP-mediated HBV entry.
CD46 represents a potential therapeutic target for treating Hepatitis B infection.