It has been over 40 years since the discovery of the “Australia antigen” in hepatitis B virus (HBV) from hemophiliac patients in 1965 by Blumberg. However, a thorough understanding of the life cycle of HBV has remained elusive so far, and there is no powerful drug for the treatment of chronic hepatitis B. The life cycle of HBV is pretty complex. The basic steps involves coupling of virus outer coat membrane with specific receptor(s) on the cell surface, entry of the virus into the cell through fusion of the viral membrane with cell membrane or phagocytosis, disassembly of the viral outer capsid in inclusion bodies, nuclear entry of core protein together with HBV DNA, which is repaired into cccDNA, and then transcription of various viral mRNAs and translation of the viral mRNAs into viral proteins for the assembly and secretion of viral particles (see Seeger C, Mason W S. Hepatitis B virus biology. Microbiol. Mol. Biol. Rev. 2000; 64:51-68). The detailed studies of HBV life cycle depends on a good HBV infection model system. Several cell lines, e.g., HepG2 and Huh-7, have been established that can support HBV replication after transfection with HBV DNA plasmids. However, transfection using HBV plasmids introduces the HBV DNA directly into these cells and does not involve the early steps of the HBV life cycle, such as virus interactions with specific cell membrane receptors, virus uncoating, and transport of the HBV DNA into the nucleus. Thus, these cell lines have limited use in the studies of the HBV life cycle. So far, only a few cells are known that can support HBV infection and replication. These cells include primary human liver cells (including embryonic liver cells), primary liver cells from tree shrew, and the recently established HepRG cells. Due to scarcity of the available sources, stringent requirements for isolation and culture conditions, and short survival time once isolated (generally less than 1 month), human primary liver cells and tree shrew primary liver cells are not suitable for scientific studies that require long-term investigation or large-scale cell culture (Guha C, Mohan S, Roy-Chowdhury N, et al. Cell culture and animal models of viral hepatitis, Part I: Hepatitis B. Lab. Anim. (NY) 2004; 33:37-46). HepRG cell line was established in 2002. This cell line is a liver progenitor cell line, which can be infected by HBV after pre-differentiation induction using DMSO. This cell line is not commercially available, but is only used in the lab where it was initially established. HepRG cells require pre-differentiation induction before they can be used in HBV infection studies. Stability and reproducibility of this model, however, are yet to be verified (see Gripon P, Rumin S, Urban S, et al. Infection of a human hepatoma cell line by the hepatitis B virus. Proc. Nat. Acad. Sci. USA. 2002; 99:1565-15660). Therefore, there is no reproducible cell line that can be used for the study of the complete HBV infection cycle. This lack of a suitable model has greatly impeded in-depth studies of various steps in the life cycle of HBV, especially the studies of the viral specific cellular receptor and the HBV DNA nuclear entry mechanism in the early stages of the HBV life cycle. The lack of a suitable cell line for HBV infection has also hindered the efforts to screen for and develop novel anti-HBV drugs. Therefore, identification of cell lines that are naturally susceptible to HBV infection remains important for the advancement of HBV research and for the development of therapeutics for chronic hepatitis.