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Glucose-regulated protein 78 is an intracellular antiviral factor against hepatitis B virus

Yan Ma1, Jun Yu, Henry L Y Chan

  • 1Stanley Ho Center for Emerging Infectious Diseases, School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong, China.

Molecular & Cellular Proteomics : MCP
|August 13, 2009
PubMed

Insights

Glucose-regulated protein 78 (GRP78) acts as an endogenous anti-Hepatitis B virus (HBV) factor. Upregulating GRP78 may offer a novel therapeutic strategy for treating HBV infection.

Area of Science:

  • Hepatology
  • Virology
  • Molecular Biology

Background:

  • Hepatitis B virus (HBV) infection is a major cause of chronic liver disease, cirrhosis, and hepatocellular carcinoma.
  • The precise mechanisms of HBV pathogenesis and host-virus interactions remain incompletely understood.
  • Identifying host factors involved in HBV replication is crucial for developing new therapies.

Purpose of the Study:

  • To investigate host protein expression changes in response to HBV replication.
  • To elucidate the role of glucose-regulated protein 78 (GRP78) in HBV infection.
  • To explore the potential of GRP78 as a therapeutic target for Hepatitis B.

Main Methods:

  • Comparative proteomics using two-dimensional gel electrophoresis and mass spectrometry on an inducible HBV-producing cell line (HepAD38).
  • Validation of differentially expressed proteins, including GRP78, using real-time RT-PCR, Western blotting, and immunohistochemistry in cell lines and human liver biopsies.
  • Functional studies involving RNA interference (knockdown) and overexpression of GRP78 in HBV-producing cells.

Main Results:

  • Twenty-three differentially expressed proteins were identified, with GRP78 significantly upregulated during HBV replication.
  • Knockdown of GRP78 enhanced HBV replication and antigen production, while GRP78 overexpression suppressed HBV.
  • GRP78 overexpression activated the interferon-beta1 (IFN-beta1)-mediated 2',5'-oligoadenylate synthetase-RNase L pathway.
  • GRP78 was downregulated in chronic hepatitis B patients post-treatment, suggesting its role in viral clearance.

Conclusions:

  • GRP78 functions as an endogenous anti-HBV factor in hepatocytes through the IFN-beta1 signaling pathway.
  • The study identifies GRP78 as a key host-virus interaction protein in HBV infection.
  • Induction of hepatic GRP78 presents a potential novel therapeutic strategy for managing HBV infection.

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