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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.

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


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.


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

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