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• W2560007443 abstract "Hepatitis B virus (HBV) infection affects 240 million people worldwide. HBV is the major cause for progressive liver diseases often leading to cirrhosis and hepatocellular carcinoma. After the isolation and genetic characterization of HBV, it became instantly clear that the virus essentially depends on species- and hepatocyte-specific host factors in its replication cycle [ [1] Seeger C. Mason W.S. Hepatitis B virus biology. Microbiol Mol Biol Rev. 2000; 64: 51-68 Crossref PubMed Scopus (1216) Google Scholar ]. Although hepatoma-derived cell lines support HBV replication and particle assembly following transfection of cloned viral genomes [ [2] Sells M.A. Zelent A.Z. Shvartsman M. Acs G. Replicative intermediates of hepatitis B virus in HepG2 cells that produce infectious virions. J Virol. 1988; 62: 2836-2844 Crossref PubMed Google Scholar ], only primary hepatocytes from humans (PHH) [ [3] Gripon P. Diot C. Theze N. Fourel I. Loreal O. Brechot C. et al. Hepatitis B virus infection of adult human hepatocytes cultured in the presence of dimethyl sulfoxide. J Virol. 1988; 62: 4136-4143 Crossref PubMed Google Scholar ] or a tree shrew [ [4] Kock J. Nassal M. MacNelly S. Baumert T.F. Blum H.E. von Weizsacker F. Efficient infection of primary tupaia hepatocytes with purified human and woolly monkey hepatitis B virus. J Virol. 2001; 75: 5084-5089 Crossref PubMed Scopus (127) Google Scholar ] support the full viral replication cycle. This includes receptor mediated entry, transport of nucleocapsids to the nucleus, rcDNA-repair and cccDNA formation. It took until 2002, when Gripon and co-workers characterized a progenitor cell line (HepaRG) from the liver of an HCV-infected patient, which – under certain culture conditions – gained susceptibility to HBV [ [5] Gripon P. Rumin S. Urban S. Le Seyec J. Glaise D. Cannie I. et al. Infection of a human hepatoma cell line by hepatitis B virus. Proc Natl Acad Sci U S A. 2002; 99: 15655-15660 Crossref PubMed Scopus (949) Google Scholar ]. These conditions included a 4-week differentiation process, leading to the formation of biliary and hepatocyte like cells (HLC). The latter resembled PHH regarding the expression of hepatocyte-specific markers such as cytochrome P450 or human albumin. After differentiation, HepaRG cells became susceptible to HBV, indicating the differentiation-dependent expression of an HBV receptor, which at that time was unknown. It took another ten years until Wenhui Li’s group from Beijing, discovered human sodium taurocholate co-transporting polypeptide (NTCP) as the long sought after HBV receptor [ [6] Yan H. Zhong G. Xu G. He W. Jing Z. Gao Z. et al. Sodium taurocholate cotransporting polypeptide is a functional receptor for human hepatitis B and D virus. Elife. 2012; 3: 28 Google Scholar ]. This finding was confirmed and consistent with the pronounced induction of NTCP expression upon differentiation of HepaRG cells [ [7] Ni Y. Lempp F.A. Mehrle S. Nkongolo S. Kaufman C. Falth M. et al. Hepatitis B and D viruses exploit sodium taurocholate co-transporting polypeptide for species-specific entry into hepatocytes. Gastroenterology. 2014; 146: 1070-1083 Abstract Full Text Full Text PDF PubMed Scopus (532) Google Scholar ]. Human stem cell-derived hepatocytes as a model for hepatitis B virus infection, spreading and virus-host interactionsJournal of HepatologyVol. 66Issue 3PreviewHepatitis B virus (HBV) remains a major public health threat with more than 240 million individuals chronically infected worldwide who are then at a high risk of developing liver cirrhosis and hepatocellular carcinoma (HCC) [1,2]. Currently, there are two classes of approved treatments: nucleos(t)ide analogs (NUC) and interferon-α (IFN-α). NUC targets viral polymerase, which limits virus replication, but cannot clear virus infection. Thus, patients need to take life-long treatment with the risk of developing drug resistance. Full-Text PDF" @default.
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• W2560007443 title "Stem cell-derived hepatocytes: A promising novel tool to study hepatitis B virus infection" @default.
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• W2560007443 doi "https://doi.org/10.1016/j.jhep.2016.11.027" @default.
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