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Primary hepatocytes of Tupaia belangeri as a potential model for hepatitis C virus infection
Xiping Zhao, … , Hubert E. Blum, Thomas F. Baumert
Xiping Zhao, … , Hubert E. Blum, Thomas F. Baumert
Published January 15, 2002
Citation Information: J Clin Invest. 2002;109(2):221-232. https://doi.org/10.1172/JCI13011.
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Article

Primary hepatocytes of Tupaia belangeri as a potential model for hepatitis C virus infection

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Abstract

Hepatitis C virus (HCV) is a major cause of chronic hepatitis worldwide, but the study of HCV infection has been hampered by the lack of an in vitro or in vivo small animal model. The tree shrew Tupaia belangeri is susceptible to infection with a variety of human viruses in vivo, including hepatitis viruses. We show that primary Tupaia hepatocytes can be infected with serum- or plasma-derived HCV from infected humans, as measured by de novo synthesis of HCV RNA, analysis of viral quasispecies evolution, and detection of viral proteins. Production of infectious virus could be demonstrated by passage to naive hepatocytes. To assess whether viral entry in Tupaia hepatocytes was dependent on the recently isolated HCV E2 binding protein CD81, we identified and characterized Tupaia CD81. Sequence analysis of cloned Tupaia cDNA revealed a high degree of homology between Tupaia and human CD81 large extracellular loops (LEL). Cellular binding of E2 and HCV infection could not be inhibited by anti-CD81 antibodies or soluble CD81-LEL, suggesting that viral entry can occur through receptors other than CD81. Thus, primary Tupaia hepatocytes provide a potential model for the study of HCV infection of hepatocytes.

Authors

Xiping Zhao, Zhen-Ya Tang, Bettina Klumpp, Guido Wolff-Vorbeck, Heidi Barth, Shoshana Levy, Fritz von Weizsäcker, Hubert E. Blum, Thomas F. Baumert

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Figure 4

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HCV protein synthesis in infected primary Tupaia hepatocytes. (a–d) Immu...
HCV protein synthesis in infected primary Tupaia hepatocytes. (a–d) Immunofluorescence of transfected primary Tupaia hepatocytes. To assess specificity and sensitivity of anti-HCV antibodies for immunofluorescence, primary Tupaia hepatocytes were cotransfected with a plasmid (pCDHCV.S1b) expressing the HCV structural proteins, and with a GFP-expression construct (pEGFP-N1) (a and b), or with pEGFP-N1 and pcDNA3 (c and d). Forty-eight hours after transfection, the cells were fixed with a 1:1 mixture of methanol/acetone (vol/vol) and incubated with a well-characterized serum panel (24, 25) from HCV-infected individuals containing high-titer anti-HCV antibody (diluted 1:100 in PBS with 1% BSA), followed by Cy3-conjugated anti–human IgG secondary antibody (b and d). To identify and locate transfected individual cells, the cells were coincubated with anti-GFP antibody, followed by an FITC-conjugated anti–rabbit IgG antibody. (a and c). (e–h) Immunofluorescence of infected Tupaia hepatocytes. For HCV infection, primary Tupaia hepatocytes were incubated with HCV RNA–positive serum 1 day after plating. On days 1 (e) and 5 (f and g) after infection, viral protein expression was analyzed by immunofluorescence using anti–HCV-specific antibodies as described above. Staining was positive in 1–5% of Tupaia hepatocytes (f and g). Anti-HCV immunoreactivity (g) could be inhibited by incubation of anti-HCV antibodies with recombinant HCV proteins prior to use in immunofluorescence (h). Magnification: ×40 (a–f) and ×10 (g and h).

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ISSN: 0021-9738 (print), 1558-8238 (online)

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