An hepatitis B and D virus infection model using human pluripotent stem cell-derived hepatocytes
Current culture systems available for studying hepatitis D virus (HDV) are suboptimal. In this study, we demonstrate that hepatocyte-like cells (HLCs) derived from human pluripotent stem cells (hPSCs) are fully permissive to HDV infection across various tested genotypes. When co-infected with the he...
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| Hauptverfasser: | , , , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
October 10, 2024
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| In: |
EMBO reports
Year: 2024, Jahrgang: 25, Heft: 10, Pages: 4311-4336 |
| ISSN: | 1469-3178 |
| DOI: | 10.1038/s44319-024-00236-0 |
| Online-Zugang: | Verlag, kostenfrei, Volltext: https://doi.org/10.1038/s44319-024-00236-0 Verlag, kostenfrei, Volltext: https://www.embopress.org/doi/full/10.1038/s44319-024-00236-0 
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| Verfasserangaben: | Huanting Chi, Bingqian Qu, Angga Prawira, Talisa Richardt, Lars Maurer, Jungen Hu, Rebecca M Fu, Florian A Lempp, Zhenfeng Zhang, Dirk Grimm, Xianfang Wu, Stephan Urban & Viet Loan Dao Thi |
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| 245 | 1 | 3 | |a An hepatitis B and D virus infection model using human pluripotent stem cell-derived hepatocytes |c Huanting Chi, Bingqian Qu, Angga Prawira, Talisa Richardt, Lars Maurer, Jungen Hu, Rebecca M Fu, Florian A Lempp, Zhenfeng Zhang, Dirk Grimm, Xianfang Wu, Stephan Urban & Viet Loan Dao Thi |
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| 520 | |a Current culture systems available for studying hepatitis D virus (HDV) are suboptimal. In this study, we demonstrate that hepatocyte-like cells (HLCs) derived from human pluripotent stem cells (hPSCs) are fully permissive to HDV infection across various tested genotypes. When co-infected with the helper hepatitis B virus (HBV) or transduced to express the HBV envelope protein HBsAg, HLCs effectively release infectious progeny virions. We also show that HBsAg-expressing HLCs support the extracellular spread of HDV, thus providing a valuable platform for testing available anti-HDV regimens. By challenging the cells along the differentiation with HDV infection, we have identified CD63 as a potential HDV co-entry factor that was rate-limiting for HDV infection in immature hepatocytes. Given their renewable source and the potential to derive hPSCs from individual patients, we propose HLCs as a promising model for investigating HDV biology. Our findings offer new insights into HDV infection and expand the repertoire of research tools available for the development of therapeutic interventions. | ||
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