2.50
Hdl Handle:
http://hdl.handle.net/10033/619035
Title:
Extra-hepatic replication and infection of hepatitis E virus in neuronal-derived cells.
Authors:
Drave, S A; Debing, Y; Walter, S; Todt, D; Engelmann, M; Friesland, M; Wedemeyer, H; Neyts, J; Behrendt, P; Steinmann, E
Abstract:
Hepatitis E virus (HEV) is the causative agent of hepatitis E in humans and a member of the genus Orthohepevirus in the family Hepeviridae. Infection usually leads to acute hepatitis that can become fulminant, particularly among pregnant women and in patients with preexisting liver disease, or may evolve to a chronic state, especially in immunosuppressed individuals. HEV has been shown to produce a range of extra-hepatic manifestations including aplastic anaemia, acute thyroiditis, glomerulonephritis as well as neurological disorders such as Guillain-Barré syndrome, neuralgic amyotrophy and encephalitis. The pathogenesis of these neurological injuries remains largely unknown, and it is also uncertain whether or not HEV can directly infect neuronal cells. In this study, we investigated whether HEV is capable of completing the viral life cycle in human neuronal-derived cell lines such as neuroepithelioma (SK-N-MC), desmoplastic cerebellar medulloblastoma (DAOY), glioblastoma multiforme (DBTRG), glioblastoma astrocytoma (U-373 MG) and oligodendrocytic (M03.13) cells. Following transfection of these cells with HEV Gaussia luciferase reporter virus, all tested cell lines supported HEV RNA replication. Furthermore, extra- and intracellular viral capsid was detected by an HEV antigen ELISA as a marker for virus assembly and release. Permissiveness for HEV cell entry could be demonstrated for the oligodendrocytic cell line M03.13. In conclusion, these results indicate that HEV tropism is not restricted to the liver and HEV can potentially complete the full viral life cycle in neuronal-derived tissues explaining neurologic disorders during HEV infection.
Affiliation:
Twincore Centre of Experimental and Clinical Infection Research; a joint venture between the Hannover Medical School and the Helmholtz Centre for Infection Research, Hannover 30625, Germany.
Citation:
Extra-hepatic replication and infection of hepatitis E virus in neuronal-derived cells. 2016, 23 (7):512-21 J. Viral Hepat.
Journal:
Journal of viral hepatitis
Issue Date:
Jul-2016
URI:
http://hdl.handle.net/10033/619035
DOI:
10.1111/jvh.12515
PubMed ID:
26891712
Type:
Article
Language:
en
ISSN:
1365-2893
Appears in Collections:
publications of the research group virus transmission ([TC]VIRT)

Full metadata record

DC FieldValue Language
dc.contributor.authorDrave, S Aen
dc.contributor.authorDebing, Yen
dc.contributor.authorWalter, Sen
dc.contributor.authorTodt, Den
dc.contributor.authorEngelmann, Men
dc.contributor.authorFriesland, Men
dc.contributor.authorWedemeyer, Hen
dc.contributor.authorNeyts, Jen
dc.contributor.authorBehrendt, Pen
dc.contributor.authorSteinmann, Een
dc.date.accessioned2016-08-30T08:51:02Z-
dc.date.available2016-08-30T08:51:02Z-
dc.date.issued2016-07-
dc.identifier.citationExtra-hepatic replication and infection of hepatitis E virus in neuronal-derived cells. 2016, 23 (7):512-21 J. Viral Hepat.en
dc.identifier.issn1365-2893-
dc.identifier.pmid26891712-
dc.identifier.doi10.1111/jvh.12515-
dc.identifier.urihttp://hdl.handle.net/10033/619035-
dc.description.abstractHepatitis E virus (HEV) is the causative agent of hepatitis E in humans and a member of the genus Orthohepevirus in the family Hepeviridae. Infection usually leads to acute hepatitis that can become fulminant, particularly among pregnant women and in patients with preexisting liver disease, or may evolve to a chronic state, especially in immunosuppressed individuals. HEV has been shown to produce a range of extra-hepatic manifestations including aplastic anaemia, acute thyroiditis, glomerulonephritis as well as neurological disorders such as Guillain-Barré syndrome, neuralgic amyotrophy and encephalitis. The pathogenesis of these neurological injuries remains largely unknown, and it is also uncertain whether or not HEV can directly infect neuronal cells. In this study, we investigated whether HEV is capable of completing the viral life cycle in human neuronal-derived cell lines such as neuroepithelioma (SK-N-MC), desmoplastic cerebellar medulloblastoma (DAOY), glioblastoma multiforme (DBTRG), glioblastoma astrocytoma (U-373 MG) and oligodendrocytic (M03.13) cells. Following transfection of these cells with HEV Gaussia luciferase reporter virus, all tested cell lines supported HEV RNA replication. Furthermore, extra- and intracellular viral capsid was detected by an HEV antigen ELISA as a marker for virus assembly and release. Permissiveness for HEV cell entry could be demonstrated for the oligodendrocytic cell line M03.13. In conclusion, these results indicate that HEV tropism is not restricted to the liver and HEV can potentially complete the full viral life cycle in neuronal-derived tissues explaining neurologic disorders during HEV infection.en
dc.language.isoenen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titleExtra-hepatic replication and infection of hepatitis E virus in neuronal-derived cells.en
dc.typeArticleen
dc.contributor.departmentTwincore Centre of Experimental and Clinical Infection Research; a joint venture between the Hannover Medical School and the Helmholtz Centre for Infection Research, Hannover 30625, Germany.en
dc.identifier.journalJournal of viral hepatitisen

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