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Front Cell Infect Microbiol. 2018 Sep 25;8:338. doi: 10.3389/fcimb.2018.00338. eCollection 2018.

The Hepatitis B Surface Antigen Binding Protein: An Immunoglobulin G Constant Region-Like Protein That Interacts With HBV Envelop Proteins and Mediates HBV Entry.

Author information

1
CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
2
The 306th Hospital of People's Liberation Army, Beijing, China.
3
Beijing YouAn Hospital, Capital Medical University, Beijing, China.
4
Laboratory of Chemical Genomics, Shenzhen Graduate School of Peking University, Shenzhen, China.
5
Savaid Medical School, University of Chinese Academy of Sciences, Beijing, China.

Abstract

Hepatitis B virus (HBV) infection is a leading cause of liver cirrhosis, liver cancer, and liver failure, affecting 350 million people worldwide. Currently available anti-HBV drugs include (PEGylated-) interferon-α and nucleos(t)ide analogs, which can cause significant side effects and drug-resistance in many cases of long-term treatment. The lack of a reliable and robust in vitro infection system is a major barrier for understanding the HBV life cycle and discovering novel therapeutic targets. In the present study, we demonstrate that overexpression of the hepatitis B surface antigen binding protein (SBP) in HepG2 cells (HepG2-SBP) resulted in their susceptibility to HBV infection. HepG2-SBP cells supported the uptake of the viral surface protein (HBsAg-preS), HBV-pseudotyped virus, and live HBV in patient sera. Moreover, SBP-mediated HBsAg-preS uptake, and HBV pseudotyped virus infections were efficiently blocked by preS1- and SBP-specific antibodies. These observations suggest that SBP is involved in HBV entry and that HepG2-SBP cells can serve as a cellular model to study the post-binding steps of HBV infection.

KEYWORDS:

HBV co-receptor; HBV entry; HBV entry cell model; hepatitis B surface antigen binding protein (SBP); hepatitis B virus (HBV)

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