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dc.contributor.authorNadeem, Abd-Elshafy D
dc.contributor.authorThomas, Pietschmann
dc.contributor.authorUlf, Müller-Ladner
dc.contributor.authorElena, Neumann
dc.contributor.authorAnggakusuma
dc.contributor.authorMohamed, Bahgat M
dc.contributor.authorFrank, Pessler
dc.contributor.authorPatrick, Behrendt
dc.date.accessioned2016-01-11T15:44:25Zen
dc.date.available2016-01-11T15:44:25Zen
dc.date.issued2015en
dc.identifier.citationCell culture-derived HCV cannot infect synovial fibroblasts. 2015, 5:18043 Sci Repen
dc.identifier.issn2045-2322en
dc.identifier.pmid26643193en
dc.identifier.doi10.1038/srep18043en
dc.identifier.urihttp://hdl.handle.net/10033/593284en
dc.description.abstractWorldwide 170 million individuals are infected with hepatitis C virus (HCV), up to 45 million of whom are affected by arthropathy. It is unclear whether this is due to viral infection of synovial cells or immune-mediated mechanisms. We tested the capacity of primary synovial fibroblasts to support HCV propagation. Out of the four critical HCV receptors, only CD81 was expressed to any significant extent in OASF and RASF. Consistent with this, pseudotyped HCV particles were unable to infect these cells. Permissiveness for HCV replication was investigated by transfecting cells with a subgenomic replicon of HCV encoding a luciferase reporter. OASF and RASF did not support replication of HCV, possibly due to low expression levels of miR-122. In conclusion, primary human synovial fibroblasts are unable to support propagation of HCV in vitro. HCV-related arthropathy is unlikely due to direct infection of these cells.
dc.language.isoenen
dc.titleCell culture-derived HCV cannot infect synovial fibroblasts.en
dc.typeArticleen
dc.contributor.departmentTWINCORE, Centre for Experimental and Clinical Infection Research GmbH, Feodor-Lynen-Str. 3-7, 30625 Hannover, Germany.en
dc.identifier.journalScientific reportsen
refterms.dateFOA2018-06-12T22:07:51Z
html.description.abstractWorldwide 170 million individuals are infected with hepatitis C virus (HCV), up to 45 million of whom are affected by arthropathy. It is unclear whether this is due to viral infection of synovial cells or immune-mediated mechanisms. We tested the capacity of primary synovial fibroblasts to support HCV propagation. Out of the four critical HCV receptors, only CD81 was expressed to any significant extent in OASF and RASF. Consistent with this, pseudotyped HCV particles were unable to infect these cells. Permissiveness for HCV replication was investigated by transfecting cells with a subgenomic replicon of HCV encoding a luciferase reporter. OASF and RASF did not support replication of HCV, possibly due to low expression levels of miR-122. In conclusion, primary human synovial fibroblasts are unable to support propagation of HCV in vitro. HCV-related arthropathy is unlikely due to direct infection of these cells.


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