Completion of hepatitis C virus replication cycle in heterokaryons excludes dominant restrictions in human non-liver and mouse liver cell lines.
Hepatitis C virus (HCV) is hepatotropic and only infects humans and chimpanzees. Consequently, an immunocompetent small animal model is lacking. The restricted tropism of HCV likely reflects specific host factor requirements. We investigated if dominant restriction factors expressed in non-liver or...
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Public Library of Science (PLoS)
2011
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oai:doaj.org-article:03bb75b6def04b5299f335b771c7e8d42021-11-18T06:03:27ZCompletion of hepatitis C virus replication cycle in heterokaryons excludes dominant restrictions in human non-liver and mouse liver cell lines.1553-73661553-737410.1371/journal.ppat.1002029https://doaj.org/article/03bb75b6def04b5299f335b771c7e8d42011-04-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21552323/pdf/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Hepatitis C virus (HCV) is hepatotropic and only infects humans and chimpanzees. Consequently, an immunocompetent small animal model is lacking. The restricted tropism of HCV likely reflects specific host factor requirements. We investigated if dominant restriction factors expressed in non-liver or non-human cell lines inhibit HCV propagation thus rendering these cells non-permissive. To this end we explored if HCV completes its replication cycle in heterokaryons between human liver cell lines and non-permissive cell lines from human non-liver or mouse liver origin. Despite functional viral pattern recognition pathways and responsiveness to interferon, virus production was observed in all fused cells and was only ablated when cells were treated with exogenous interferon. These results exclude that constitutive or virus-induced expression of dominant restriction factors prevents propagation of HCV in these cell types, which has important implications for HCV tissue and species tropism. In turn, these data strongly advocate transgenic approaches of crucial human HCV cofactors to establish an immunocompetent small animal model.Anne FrentzenKathrin HügingJulia BitzegeioMartina FrieslandSibylle HaidJuliane GentzschMarkus HoffmannDirk LindemannGert ZimmerFlorian ZieleckiFriedemann WeberEike SteinmannThomas PietschmannPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 7, Iss 4, p e1002029 (2011) |
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DOAJ |
| collection |
DOAJ |
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| topic |
Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 |
| spellingShingle |
Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Anne Frentzen Kathrin Hüging Julia Bitzegeio Martina Friesland Sibylle Haid Juliane Gentzsch Markus Hoffmann Dirk Lindemann Gert Zimmer Florian Zielecki Friedemann Weber Eike Steinmann Thomas Pietschmann Completion of hepatitis C virus replication cycle in heterokaryons excludes dominant restrictions in human non-liver and mouse liver cell lines. |
| description |
Hepatitis C virus (HCV) is hepatotropic and only infects humans and chimpanzees. Consequently, an immunocompetent small animal model is lacking. The restricted tropism of HCV likely reflects specific host factor requirements. We investigated if dominant restriction factors expressed in non-liver or non-human cell lines inhibit HCV propagation thus rendering these cells non-permissive. To this end we explored if HCV completes its replication cycle in heterokaryons between human liver cell lines and non-permissive cell lines from human non-liver or mouse liver origin. Despite functional viral pattern recognition pathways and responsiveness to interferon, virus production was observed in all fused cells and was only ablated when cells were treated with exogenous interferon. These results exclude that constitutive or virus-induced expression of dominant restriction factors prevents propagation of HCV in these cell types, which has important implications for HCV tissue and species tropism. In turn, these data strongly advocate transgenic approaches of crucial human HCV cofactors to establish an immunocompetent small animal model. |
| format |
article |
| author |
Anne Frentzen Kathrin Hüging Julia Bitzegeio Martina Friesland Sibylle Haid Juliane Gentzsch Markus Hoffmann Dirk Lindemann Gert Zimmer Florian Zielecki Friedemann Weber Eike Steinmann Thomas Pietschmann |
| author_facet |
Anne Frentzen Kathrin Hüging Julia Bitzegeio Martina Friesland Sibylle Haid Juliane Gentzsch Markus Hoffmann Dirk Lindemann Gert Zimmer Florian Zielecki Friedemann Weber Eike Steinmann Thomas Pietschmann |
| author_sort |
Anne Frentzen |
| title |
Completion of hepatitis C virus replication cycle in heterokaryons excludes dominant restrictions in human non-liver and mouse liver cell lines. |
| title_short |
Completion of hepatitis C virus replication cycle in heterokaryons excludes dominant restrictions in human non-liver and mouse liver cell lines. |
| title_full |
Completion of hepatitis C virus replication cycle in heterokaryons excludes dominant restrictions in human non-liver and mouse liver cell lines. |
| title_fullStr |
Completion of hepatitis C virus replication cycle in heterokaryons excludes dominant restrictions in human non-liver and mouse liver cell lines. |
| title_full_unstemmed |
Completion of hepatitis C virus replication cycle in heterokaryons excludes dominant restrictions in human non-liver and mouse liver cell lines. |
| title_sort |
completion of hepatitis c virus replication cycle in heterokaryons excludes dominant restrictions in human non-liver and mouse liver cell lines. |
| publisher |
Public Library of Science (PLoS) |
| publishDate |
2011 |
| url |
https://doaj.org/article/03bb75b6def04b5299f335b771c7e8d4 |
| work_keys_str_mv |
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1718424644810178560 |