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Epidermal growth factor receptor is a host-entry cofactor triggering hepatitis B virus internalization.

Masashi Iwamoto1,2, Wakana Saso1,3, Ryuichi Sugiyama1

  • 1Department of Virology II, National Institute of Infectious Diseases, 162-8640 Tokyo, Japan.

Proceedings of the National Academy of Sciences of the United States of America
|April 7, 2019
PubMed
Summary

Epidermal growth factor receptor (EGFR) is crucial for hepatitis B virus (HBV) entry into cells expressing sodium taurocholate cotransporting polypeptide (NTCP). EGFR mediates HBV internalization, linking cell surface attachment to viral invasion.

Keywords:
EGFRHBVNTCPentrytransporter

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Area of Science:

  • Hepatology
  • Virology
  • Cell Biology

Background:

  • Sodium taurocholate cotransporting polypeptide (NTCP) is essential for hepatitis B virus (HBV) entry.
  • Cell susceptibility to HBV varies with culture conditions, with epidermal growth factor (EGF) enhancing infection.
  • The precise mechanism linking cell surface attachment to viral internalization remains unclear.

Purpose of the Study:

  • To investigate the role of epidermal growth factor receptor (EGFR) in HBV virion internalization.
  • To elucidate the interaction between NTCP and EGFR in the context of HBV entry.

Main Methods:

  • Utilized EGFR-knockdown cells to assess HBV and preS1 peptide internalization.
  • Employed EGFR complementation assays to rescue viral entry.
  • Performed immunoprecipitation assays to document NTCP-EGFR molecular interaction.
  • Investigated the impact of NTCP mutations, decoy peptides, and EGFR inactivation on viral infection.

Main Results:

  • EGFR knockdown attenuated HBV and preS1 peptide internalization.
  • Functional EGFR expression rescued preS1 internalization and HBV infection.
  • HBV/preS1-NTCP complex internalization correlated with EGFR endocytotic relocalization.
  • Disruption of NTCP-EGFR interaction abrogated NTCP's function in supporting HBV infection.

Conclusions:

  • EGFR plays a critical role in mediating the internalization of the HBV/NTCP complex into susceptible cells.
  • EGFR acts as a crucial link between cell-surface HBV-NTCP attachment and viral invasion.
  • Targeting the NTCP-EGFR interaction could offer novel strategies for inhibiting HBV entry.