Extra-hepatic replication and infection of hepatitis E virus in neuronal-derived cells
2016
Summary
Hepatitis E virus(HEV) is the causative agent of
hepatitis Ein humans and a member of the genus
Orthohepevirusin 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 disorderssuch as
Guillain-Barre syndrome, neuralgic
amyotrophyand encephalitis. The pathogenesis of these
neurological injuriesremains 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 cyclein 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
Gaussialuciferase 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
oligodendrocyticcell line M03.13. In conclusion, these results indicate that HEV
tropismis not restricted to the liver and HEV can potentially complete the full
viral life cyclein neuronal-derived tissues explaining
neurologic disordersduring HEV infection.
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